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FDA approves new type 2 diabetes drug bexagliflozin
The U.S. Food and Drug Administration has approved bexagliflozin (Brenzavvy, TheracosBio) for the treatment of adults with type 2 diabetes.
The once-daily 20-mg oral sodium-glucose cotransporter 2 (SGLT2) inhibitor is indicated as an adjunct to diet and exercise to improve glycemic control for those with type 2 diabetes, but not type 1 diabetes. It can be used in adults with an estimated glomerular filtration rate (eGFR) > 30 mL/min per 1.73 m2.
Approval was based on results from 23 clinical trials with more than 5,000 participants, including more than 300 patients with stage 3 kidney disease (eGFR < 60 and > 30 mL/min per 1.73 m2).
In the phase 3 studies, bexagliflozin significantly reduced hemoglobin A1c and fasting blood glucose at 24 weeks as monotherapy or as add-on to metformin and other glucose-lowering drugs and combinations. It also produced modest reductions in body weight and systolic blood pressure.
In the phase 3 Bexagliflozin Efficacy and Safety Trial (BEST) cardiovascular outcomes trial, the drug met its efficacy and safety objectives in patients at high cardiovascular risk. Noninferiority was demonstrated for the composite outcome of cardiovascular death, myocardial infarction, stroke, or unstable angina.
“As a class of drugs, SGLT2 inhibitors have shown tremendous benefit in treating adults with type 2 diabetes,” said Mason Freeman, MD, director of the Translational Research Center at Massachusetts General Hospital, Boston, in a press release from TheracosBio.
“Being involved in all of the clinical trials for Brenzavvy, I am greatly impressed with the efficacy of the drug in reducing blood glucose levels and I believe it is an important addition to the SGLT2 inhibitor class of drugs.”
As with other SGLT2 inhibitors, adverse events seen in the trials include ketoacidosis, lower limb amputation, volume depletion, urosepsis, pyelonephritis, Fournier’s gangrene, genital mycotic infections, and hypoglycemia when used with insulin or insulin secretagogues.
Bexagliflozin joins an already crowded field of SGLT2 inhibitors, some of which have been approved for additional cardiovascular and kidney indications.
Of interest, bexagliflozin was approved by the FDA for diabetes in cats in December 2022, as the first oral new animal drug to improve glycemic control in otherwise healthy cats with diabetes not previously treated with insulin.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration has approved bexagliflozin (Brenzavvy, TheracosBio) for the treatment of adults with type 2 diabetes.
The once-daily 20-mg oral sodium-glucose cotransporter 2 (SGLT2) inhibitor is indicated as an adjunct to diet and exercise to improve glycemic control for those with type 2 diabetes, but not type 1 diabetes. It can be used in adults with an estimated glomerular filtration rate (eGFR) > 30 mL/min per 1.73 m2.
Approval was based on results from 23 clinical trials with more than 5,000 participants, including more than 300 patients with stage 3 kidney disease (eGFR < 60 and > 30 mL/min per 1.73 m2).
In the phase 3 studies, bexagliflozin significantly reduced hemoglobin A1c and fasting blood glucose at 24 weeks as monotherapy or as add-on to metformin and other glucose-lowering drugs and combinations. It also produced modest reductions in body weight and systolic blood pressure.
In the phase 3 Bexagliflozin Efficacy and Safety Trial (BEST) cardiovascular outcomes trial, the drug met its efficacy and safety objectives in patients at high cardiovascular risk. Noninferiority was demonstrated for the composite outcome of cardiovascular death, myocardial infarction, stroke, or unstable angina.
“As a class of drugs, SGLT2 inhibitors have shown tremendous benefit in treating adults with type 2 diabetes,” said Mason Freeman, MD, director of the Translational Research Center at Massachusetts General Hospital, Boston, in a press release from TheracosBio.
“Being involved in all of the clinical trials for Brenzavvy, I am greatly impressed with the efficacy of the drug in reducing blood glucose levels and I believe it is an important addition to the SGLT2 inhibitor class of drugs.”
As with other SGLT2 inhibitors, adverse events seen in the trials include ketoacidosis, lower limb amputation, volume depletion, urosepsis, pyelonephritis, Fournier’s gangrene, genital mycotic infections, and hypoglycemia when used with insulin or insulin secretagogues.
Bexagliflozin joins an already crowded field of SGLT2 inhibitors, some of which have been approved for additional cardiovascular and kidney indications.
Of interest, bexagliflozin was approved by the FDA for diabetes in cats in December 2022, as the first oral new animal drug to improve glycemic control in otherwise healthy cats with diabetes not previously treated with insulin.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration has approved bexagliflozin (Brenzavvy, TheracosBio) for the treatment of adults with type 2 diabetes.
The once-daily 20-mg oral sodium-glucose cotransporter 2 (SGLT2) inhibitor is indicated as an adjunct to diet and exercise to improve glycemic control for those with type 2 diabetes, but not type 1 diabetes. It can be used in adults with an estimated glomerular filtration rate (eGFR) > 30 mL/min per 1.73 m2.
Approval was based on results from 23 clinical trials with more than 5,000 participants, including more than 300 patients with stage 3 kidney disease (eGFR < 60 and > 30 mL/min per 1.73 m2).
In the phase 3 studies, bexagliflozin significantly reduced hemoglobin A1c and fasting blood glucose at 24 weeks as monotherapy or as add-on to metformin and other glucose-lowering drugs and combinations. It also produced modest reductions in body weight and systolic blood pressure.
In the phase 3 Bexagliflozin Efficacy and Safety Trial (BEST) cardiovascular outcomes trial, the drug met its efficacy and safety objectives in patients at high cardiovascular risk. Noninferiority was demonstrated for the composite outcome of cardiovascular death, myocardial infarction, stroke, or unstable angina.
“As a class of drugs, SGLT2 inhibitors have shown tremendous benefit in treating adults with type 2 diabetes,” said Mason Freeman, MD, director of the Translational Research Center at Massachusetts General Hospital, Boston, in a press release from TheracosBio.
“Being involved in all of the clinical trials for Brenzavvy, I am greatly impressed with the efficacy of the drug in reducing blood glucose levels and I believe it is an important addition to the SGLT2 inhibitor class of drugs.”
As with other SGLT2 inhibitors, adverse events seen in the trials include ketoacidosis, lower limb amputation, volume depletion, urosepsis, pyelonephritis, Fournier’s gangrene, genital mycotic infections, and hypoglycemia when used with insulin or insulin secretagogues.
Bexagliflozin joins an already crowded field of SGLT2 inhibitors, some of which have been approved for additional cardiovascular and kidney indications.
Of interest, bexagliflozin was approved by the FDA for diabetes in cats in December 2022, as the first oral new animal drug to improve glycemic control in otherwise healthy cats with diabetes not previously treated with insulin.
A version of this article first appeared on Medscape.com.
Damar Hamlin’s cardiac arrest: Key lessons
This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.
Dr. Pepe: Thanks for having us here.
Dr. Glatter: the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.
Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.
Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?
Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.
More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.
When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.
Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.
In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?
Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.
In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.
I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.
As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.
Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.
Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.
Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.
I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.
Dr. Glatter: How to turn it on, where it is, and how to operate it.
Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.
Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?
Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.
From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.
Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.
The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.
The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.
Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.
Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.
It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.
Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.
That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.
Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.
Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.
Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.
The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.
Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.
I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.
Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.
Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.
Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.
We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”
I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”
That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.
A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.
Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.
The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.
The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.
Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.
For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”
With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.
Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.
Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.
Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.
Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.
I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.
Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.
Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.
Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.
Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.
Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.
Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.
Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.
A version of this article first appeared on Medscape.com.
This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.
Dr. Pepe: Thanks for having us here.
Dr. Glatter: the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.
Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.
Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?
Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.
More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.
When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.
Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.
In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?
Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.
In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.
I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.
As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.
Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.
Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.
Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.
I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.
Dr. Glatter: How to turn it on, where it is, and how to operate it.
Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.
Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?
Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.
From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.
Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.
The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.
The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.
Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.
Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.
It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.
Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.
That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.
Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.
Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.
Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.
The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.
Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.
I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.
Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.
Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.
Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.
We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”
I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”
That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.
A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.
Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.
The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.
The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.
Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.
For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”
With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.
Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.
Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.
Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.
Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.
I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.
Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.
Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.
Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.
Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.
Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.
Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.
Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.
A version of this article first appeared on Medscape.com.
This discussion was recorded on Jan. 9, 2023. This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr. Robert D. Glatter, medical adviser for Medscape Emergency Medicine. Today, we have Dr. Paul E. Pepe, an emergency medicine physician based in Florida and a highly recognized expert in emergency medical services (EMS), critical care, sports and event medicine, and resuscitation. Also joining us is Dr. Michael S. (“Mick”) Malloy, an emergency medicine physician based in Ireland, also an expert in prehospital care, resuscitation, and sports and event medicine. Welcome, gentlemen.
Dr. Pepe: Thanks for having us here.
Dr. Glatter: the Buffalo Bills safety who went down suffering a cardiac arrest in front of millions of people. Although we don’t know the exact cause of the events that transpired, the goal of our discussion is to guide our audience through a systematic approach to evaluation and management of an athlete suffering blunt force chest and neck trauma, and then suffering a cardiac arrest. We do know, obviously, that Damar was successfully resuscitated, thanks to the medical staff and trainers.
Almost 50 years ago, Chuck Hughes, a Detroit Lions receiver, went down and died with just a minute to go in the game and, unfortunately, didn’t survive.
Paul, can you tell me your impressions after viewing the replay of the events that evening? What were the most likely causes of this syncopal event and the subsequent cardiac arrest?
Dr. Pepe: We don’t know anything specifically. It’s being kept private about what the events were. It’s a little bit complicated in a sense that he basically had an extended resuscitation in the hospital. My experience has been that most people that have ventricular fibrillation, from whatever cause, will most likely be waking up on the field if you get to them. I’ve had personal experience with that.
More importantly than when it starts, when someone goes down on the field, both Dr. Malloy and I take a broader view. We don’t get tunnel vision and think, “Oh, it was a traumatic event,” or “It was cardiac event,” and we just have our minds open. There are many things that could make you stop breathing on the field. It could be a neck or a severe head injury, and then any kind of other internal injury that occurs.
When I saw in the video that Damar Hamlin stood up, that made it a less likely to be a spinal injury. He seemed to be physically functioning, and then he suddenly collapsed. That went along with something that looks like a ventricular fibrillation or ventricular tachycardia type of event and made me think right away that it was commotio cordis. I’m not a Latin scholar, but commotio is like commotion. A literal translation might be an agitation of the heart. I was thinking that he probably got hit somewhere in the middle of the chest at the right moment where the heart is resetting in that repolarization phase, like an R-on-T phenomenon, and then caused this sudden ventricular dysrhythmia.
Most people associate it to that because we have a couple of dozen cases a year of people getting hockey pucks or a baseball hitting their chest, which is very common with adolescents. On the other hand, you can’t get it from a blunt injury like this, and it was too early for it to be, say, a direct cardiac contusion, unless there was a direct injury there. It just happened so quickly.
In Europe, they’ve had a large amount of experience with this same kind of problem before, even just from a direct shoulder hit, for example. Mick Malloy is the dean of the faculty of sports and exercise medicine at the Royal College of Surgeons in Ireland and has vast experience, and now he is the person overseeing the procedures for this. Mick, have you had those kinds of experiences as well?
Dr. Molloy: Yes. It’s something that has occurred over recent decades and has been more recognized. I note that in professional sports, it’s a very different thing because you’ve got such huge teams and teams trained to respond very quickly. And that’s the most important thing in this scenario – having a team that is well functioning as a high-class emergency response team ready to get out on to that field very quickly after the person collapses, getting the automated external defibrillator (AED) on, and then recognizing whether there needs to be a shock given or not. The machine will tell you all that.
In our scenario, we run courses called CARES (Care of the Athlete Resuscitation and Emergencies in Sport) to make sure that our team physicians and team physiotherapists and trainers are all speaking as one when an emergency arises.
I don’t worry so much about the professional sport. It’s more with the amateur sports and the kids sports that I get a bit more concerned because there isn’t the same level of medical care there. Having everybody trained in basic life support would be very important to reduce unnecessary deaths from these types of conditions.
As Paul mentioned, there is a very specific cardiac cause in some of these circumstances, where you get hit just at the wrong time and that hit occurs at a particular electrical point in time. It causes this ventricular fibrillation, and the only real treatment there is the defibrillator as quickly as possible.
Dr. Glatter: What you’re saying ultimately is an important part about rapid defibrillation, and at first, cardiopulmonary resuscitation (CPR). People are concerned about whether they should begin CPR. We’re talking about out-of-hospital cardiac arrest that is outside of a football stadium, for example. Some people are obsessed with taking a person’s pulse, and that’s been a point of contention. If someone is unconscious and not breathing, we should start CPR. Wouldn›t you agree? They will wake up quickly if you begin chest compressions if they’re not necessary.
Dr. Pepe: I tell people, just do it. You’re right, people will wake up and feel it if they don’t need it.
Getting back to Mick’s point of having things ready to go, for example, 8 years ago, we had a professional player on the bench who suddenly collapsed right there in front of the entire audience. We immediately did CPR, and we got the AED on. We shocked him and he was ready, willing, and able to get back on the bench again. It turns out he had underlying coronary artery disease, but we got him back right away.
I did an initial study where we placed an AED in a public place at the Chicago O’Hare Airport to see if the public would use these. Most cardiac arrests occur at home, of course, but in public places, that was a good place to try it. We had almost 10 cases the first year. What was fascinating was that we had almost no survivors over the previous decade, even though there were paramedics at the airport. When we put these out there, we had nine people go down that first year, and six people who had never operated an AED or seen one before knew to get one and use it. Every one of those people survived neurologically intact, and almost every person was waking up before traditional responders got there. That’s how effective this is, but you need to know where the AED is.
Dr. Glatter: How to turn it on, where it is, and how to operate it.
Dr. Pepe: That was the point: These rescuers saved lives in the first year, and it was tremendous. Two points I make about it are that one, you need to know where it is, and two, just go turn it on. It gives you the instructions to follow through; just be in the Nike mode, because it basically won’t hurt a person. It’s rare that there’s ever been any complication of that. The machine algorithms are so good.
Dr. Glatter: Mick, I want to turn to you about the European experience. Specifically in Denmark, we know that there’s a large public health initiative to have AEDs accessible. There have been studies showing that when the public is engaged, especially with studies looking at an app when access is available, survivability doubled in the past 10 years from having access to AEDs. What’s your experience in Ireland in terms of public access to defibrillators?
Dr. Molloy: We’ve got two different streams here. There was a big push to have more AEDs at all sports venues. That was great, but some of the sporting clubs put them inside the locked door. I said that there’s no point to that because nobody can access it. You need to have an external building and you need to leave it open. If somebody needs to use it, they need to know how to get it, open it, and get away, and not get in through a locked door to get access to a defibrillator. We have AEDs now in most stadiums and even in small rural areas, where you might have only 200 people turn up for a game.
From another public access side, if you dial in – in our scenario, it’s 112, not 911 –we have Community First Responder groups. In the rural areas, you have local people who’ve been trained in basic life support and community first response who have AEDs. They’ll have periods of the day where they come home from work as a teacher, a nurse, a policeman, or a fireman, and they turn on an app on their phone and say, “I’m available for the next 5 hours.” If there’s a cardiac arrest rung in within 5 miles of their community, they will drive directly there with the AED that they have. We’ve had numerous saves from that in the country because it could take 40 minutes to get an EMS vehicle there, and obviously, time is crucial in these scenarios. Our dispatchers will talk people through CPR, and then the community responders arrive with the AED. It has been a fantastic initiative.
Dr. Pepe: In many places, people have apps on their phones where they’re locked into the system, and it will go off and tell them there is something nearby and even GPS them into it, and it’s been fantastic.
The two points I want to make to responding to what we just heard Dean Malloy say is one, we always have a designated spot to have these in various places. If I’m at City Hall, we always have them near the red elevators on every floor and down at security. In all the public high schools, we always have one right below the clock where everybody can see it. We set it up in a very standardized form that anybody and everybody will know where it is at the time an event happens.
The other point he made about having the response teams is fantastic. I live in a large high rise and there are two complexes with many people here, and many are older, so there’s going to be a higher risk for having an event. In fact, we’ve just had one recently. The concept we developed here was a community emergency response team, where we sometimes have doctors, nurses, and paramedics who live here be on call and be responsible, or you could try to find an AED. More importantly, we made sure everybody here knew where they were and where to get them. We’ve got most of the people trained, and we’re doing more training in what actions to take during these periods of time when such events happen.
Dr. Glatter: Yes, it’s critical. I wanted to point out that we’ve looked at the use of drones, especially here in the United States. There have been some pilot studies looking at their utility in the setting of out-of-hospital cardiac arrest. I want to get both of your thoughts on this and the feasibility of this.
Dr. Molloy: In a rural area, it’s a fantastic idea. You’re going to get something there as the crow flies very quickly. You probably have to look at exactly in, say, a rural area like Ireland of 32,000 square kilometers, how many you›ll have to put, what kind of distances they can realistically cover, and make sure the batteries are charged. Certainly, that’s a very good initiative because with the AEDs, you can’t do anything wrong. You can’t give a shock unless a shock needs to be given. The machine directs you what to do, so somebody who has had no training can pick one of these out of the box and start to work with it quickly and confidently that they can’t do anything wrong.
It’s a great idea. It would be a little expensive potentially at the moment in getting the drones and having that volume of drones around. In the U.S., you have completely different air traffic than we have, and in cities, you have more helicopters flying around. We certainly wouldn’t have that in our cities because that could cause a challenge if you’ve got drones flying around as well. It’s about making it safe that nothing else can go wrong from a drone in somebody else’s flight path.
Dr. Pepe: In my experience, the earlier the intervention, the better the results. There is a limit here in terms of the drones if they just can’t get there soon enough. Having said that, we are so fortunate in the city of Seattle to have most citizens knowing CPR, and we’d get that person resuscitated because they were doing such a good job with the CPR up front.
That’s why you’re going to see the Buffalo Bills player survive neurologically intact – because he did get immediate treatment right then and there. In the future, we may even have some better devices that will actually even restore normal blood flow right then and there while you’re still in cardiac arrest. There are limitations in every case. But on the other hand, it’s exciting and it paid off in this case recently.
Dr. Molloy: Just a point of interest coming from this small little country over here. The first portable defibrillator was developed in Belfast, Ireland, in the back of a cardiac response car. Despite us being a tiny little country, we do have some advances ahead of the United States.
Dr. Pepe: That was a breakthrough. Dr. Frank Pantridge and John Geddes did this great work and that caught the imagination of everybody here. At first, they were just going out to give people oxygen and sedate them for their chest pain. It turned out that their defibrillators are what made the difference as they went out there. Absolutely, I have to acknowledge the folks in Ireland for giving us this. Many of the EMS systems got started because of the article they published in The Lancet back in 1967.
Dr. Glatter: I wanted to briefly talk about screening of the athletes at the high school/college level, but also at the professional level. Obviously, there are issues, including the risk for false-positives in terms of low incidence, but there are also false negatives, as the case with Christian Eriksen, who had a cardiac arrest in 2021 and who has been through extensive testing. We can debate the validity of such testing, but I wanted to get both of your takes on the utility of screening in such a population.
Dr. Molloy: That’s a very emotive subject. False-positives are difficult because you’re now saying to somebody that they can’t compete in your sport at a decent level. The difficult part is telling somebody that this is the end of their career.
The false-negative is a little bit more difficult. I don’t know Christian Eriksen and I’m not involved in his team in any way, but that is a one-point examination, and you’re dependent on the scale of the process interpreting the ECG, which is again only a couple of seconds and that particular arrhythmia may not have shown up on that.
Also, athletes, by nature of what they’re doing, are operating at 99% of efficiency on a frequent basis. They are at the peak of their physiologic fitness, and it does make them a little bit more prone to picking up viral illnesses from time to time. They may get a small viral myopericarditis, which causes a new arrhythmia that nobody knew about. They had the screening 2 or 3 years ago, and they now developed a new problem because of what they do, which just may not show up.
I was actually surprised that the gentleman came through it very well, which is fantastic. He wasn’t allowed to play football in the country where he was employed, and he has now moved to another country and is playing football with a defibrillator inserted. I don’t know what the rules are in American football where you can play with implantable defibrillators. I’m not so sure it’s a great idea to do that.
Dr. Pepe: One thing that we should bring up is that there are athletes with underlying cardiomyopathies or hypertrophies and things like that, but that was unlikely in this case. It’s possible, but it’s unlikely, because it would have manifested itself before. In terms of screening, I’ve met some very smart medical doctors who have run those tests, and they have been very encouraged even at the high school levels to have screenings done, whether it’s electrocardiography, echocardiography, and so on. I have to reiterate what Dr Malloy just said in that it may have its downsides as well. If you can pick up real obvious cases, I think that may be of value.
Dr. Glatter: I want to conclude and get some pearls and takeaways from each of you regarding the events that transpired and what our audience can really hold onto.
Dr. Molloy: Look at Formula One in the past 50 years. In Formula One, in the beginning it was a 2-minute job to change a tire. Now, they have this down where they’re measuring in fractions of a second and criticizing each other if one guy is 2.6 seconds and the other guy is 2.9 seconds. For me, that’s phenomenal. It takes me 25 minutes to change a tire.
We’ve looked at that from a resuscitation perspective, and we now do pit crew resuscitation before our events. We’ve planned our team and know who’s going to be occupying what role. After the events at the UEFA championships, we had a new rule brought in by UEFA where they handed me a new document saying, “This is what we would like you to do for resuscitation.” It was a three-man triangle, and I said, “No, we’re not going to do that here.” And they said, “Why, you have to; it’s our rule.”
I said, “No, our rule in Ireland is we have a six-person triangle. We’re not downing our standards because of what you have internationally. You’re covering games in some very low-resource environments, I know that. We have a particular standard here that we’re sticking to. We have a six-person group. We know what we’re all doing; we come very quickly to those downed players and get involved and we’ve had good outcomes, so we’re not going to change the standards.”
That’s the thing: You need to practice these things. The players don’t go out on the weekend and do a move for the very first time without practicing it hundreds of times. We need to look at it the same way as the medical team who are looking after that group of players and the crowd because we also look after the crowd.
A particular challenge in some of our stadiums is that the upper decks are so steep, and it’s very hard to get a patient onto a trolley and do CPR as you’re bringing them down to a zone to get them flat. We’ve had to come up with some innovative techniques to try and do that and accommodate that using some of the mechanical CPR devices. That’s the result you’ll only get from having practiced these events and trying to extricate patients. We want to check response times, so you have to practice your response team activity very frequently.
Dr. Pepe: There are two points made by Mick that I want to react to. One, the pit crew approach is critical in so many ways. We do the same thing in what we call the medical first attack, where we knew who the A, B, and C person would be. When we took it out to the NBA trainers, I recommended for them to have a similar approach so that if an event does happen right in the middle of prime time, they are coordinated.
The second point is that we do mass-gathering medicine. It’s not just the sportspeople on the field or the entertainers that we’re looking after; it is the people in the stands. We will see a cardiac arrest once a month. If you think about it, you might see a cardiac arrest occur in any community on a regular basis. Now you’ve got 100,000 people in one stadium, and something is bound to go wrong over those 3 or 4 hours where they are there and may have a critical emergency. Preparation for all of that is really important as well.
The final point is that on a day-to-day basis, most cardiac arrests do occur in the home. Granted, 80% of them are nonshockable cases, but the people who are more apt to survive are going to be the ones who have an electrical event. In fact, when we looked at our data years ago, we found that, of the cases of people with ventricular fibrillation that we resuscitated, half didn’t even have heart damage. Their enzymes were normal. It was a pure electrical event, and they were more resuscitable. They may have an underlying problem, but we can fix that once we get them back.
Everybody needs to know how to do bystander CPR, and second, we must make sure we have AEDs strategically placed, as I alluded to before. We also go out to other parts of the community and give them advice. All those things must be put in place, but more importantly, just get the training and make the training simple. It’s really a “just do it” philosophy, but make it simple.
For example, when I teach a course, I can do it in 15 minutes, and people retain it because I keep reiterating things like, “Okay, there’s one thing you need to know about choking: Pop the cork.” You give them a physiologic image of what’s happening. Everybody says, “I remember you saying to just do it, pop the cork.”
With AEDs, know where it is – that’s why we should have it in standardized places. Go get it, turn it on, and then follow the instructions. Also, the most important thing is making sure you’re doing quality compressions; and there are videos that can help you with that, as well as classes that you can take that will get you through it.
Dr. Glatter: Absolutely. The public still has the misconception that you need to do mouth-to-mouth resuscitation. The message has not permeated through society that you don’t need to do mouth-to-mouth. Hands-only CPR is the gold standard now.
Dr. Pepe: If people have a reversible cause like ventricular fibrillation, often they’re already gasping, which is better than a delivered breath, by the way. Most important, then, are the compressions to make sure you have oxygen going up to the brain, because you’re still theoretically loaded with oxygen in your bloodstream if you had a sudden cardiac arrest from a ventricular fibrillation.
Your points are well taken, and we found that we had better outcomes when we just gave instructions to do compressions only, and that became the standard. Mick, you’ve had some experiences with that as well.
Dr. Molloy: If we’re going to have a long-term benefit from all this, we have to start doing this in elementary school and teaching kids basic life support and some basic health messaging.
I remember trying to get this across to a teacher one day and the teacher saying, “But why would we teach young kids to resuscitate each other?” I said, “I think you forget that the only 60-year-old person in the room is you. You train them, and we train them. They’re the ones who are going to respond and keep you alive. That’s the way you should be looking at this.” That completely changed the mindset of whether we should be doing this for the kids or not.
Dr. Pepe: In fact, what we find is that that’s exactly who gets saved. I had case after case where the kids at the school had learned CPR and saved the teachers or the administrator at the high school or elementary school. It’s a fantastic point that you bring up, Dr. Malloy.
Dr. Glatter: One other brief thing we can interject here is that the team was excellent on field in that they evaluated Damar Hamlin in a primary survey sense of ABCs (i.e., airway, breathing, and circulation) for things like a tension pneumothorax. In the sense in which he was hit, there are reversible causes. Making sure he didn’t have a tension pneumothorax that caused the arrest, in my mind, was critical.
Dr. Pepe: We do the same thing on a day-to-day basis with a car wreck, because it could be that the person had ventricular fibrillation and then had the wreck. It’s not always trauma. That’s a fantastic point that you’re making. That’s exactly what I think happened, and that’s what we do.
Dr. Glatter: Well, thank you, gentlemen. This was an informative and helpful discussion for our audience. I appreciate your time and expertise.
Dr. Glatter, is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York. He is an editorial adviser and hosts the Hot Topics in EM series on Medscape. He is also a medical contributor for Forbes.
Dr. Pepe is a professor of internal medicine, surgery, pediatrics, public health, and emergency medicine at University of Texas Health Science Center in Houston. He’s also a global coordinator of the U.S. Metropolitan Municipalities EMS Medical Directors (“Eagles”) Coalition.
Dr. Molloy works clinically as a consultant in emergency medicine in Wexford General Hospital, part of the Ireland East Hospital Group (IEHG). Internationally, he is a member of the Disaster Medicine Section of the European Society of Emergency Medicine (EUSEM) and has been appointed by the Irish Medical Organization (IMO) as one of two Irish delegates to serve on the European Board and Section of Emergency Medicine of the European Union of Medical Specialists (UEMS), having served for a number of years on its predecessor, the Multidisciplinary Joint Committee on Emergency Medicine.
A version of this article first appeared on Medscape.com.
Emotional eating tied to risk of diastolic dysfunction
Eating in response to stress – known as emotional eating – was significantly associated with several markers of long-term cardiovascular damage, based on data from 1,109 individuals.
“We know diet plays a huge role in cardiovascular disease, but we have focused a lot of work on what you eat, not on what makes you eat” – the current study did exactly that, Martha Gulati, MD, who wasn’t involved in the study, said in an interview.
“Emotional eaters consume food to satisfy their brains rather than their stomachs,” study investigator Nicolas Girerd, MD, of the National Institute of Health and Medical Research (INSERM) and a cardiologist at the University Hospital of Nancy (France), wrote in a press release accompanying the study.
Diet plays a role in the development of cardiovascular disease (CVD), but the impact of eating behavior on long-term cardiovascular health remains unclear, wrote Dr. Girerd and colleagues. Previous research has yielded three common psychological dimensions for eating behavior: emotional eating, restrained eating, and external eating.
Both emotional eating and restrained eating have been linked to cardiovascular disease risk, the researchers noted. “Because of previous findings, we hypothesized that [emotional and/or restrained dimensions of eating behavior] are positively associated with cardiovascular damages, as well as with CV risk factors, such as metabolic syndrome,” they wrote.
In a study published in the European Journal of Preventive Cardiology, the researchers reviewed data from 916 adults and 193 adolescents who were participants in the STANISLAS (Suivi Temporaire Annuel Non-Invasif de la Santé des Lorrains Assurés Sociaux), a longitudinal familial cohort in France. Cardiovascular data were collected at four medical visits as part of a full clinical examination between 1993 and 2016, with one visit every 5-10 years. Roughly one-third (31.0%) of the adults were overweight, 7.9% were obese, and 2.7% were underweight. The median age of the adults at the second visit was 44.7 years; the median age of the adolescent group was 15.2 years.
The primary outcome of cardiovascular damage was measured at the fourth visit. Eating behavior was assessed during the second visit using the Dutch Eating Behaviour Questionnaire (DEBQ), and participants were identified as emotional eaters, restrained eaters, or external eaters.
Among the adults, emotional eating was associated with a 38% increased risk of diastolic dysfunction (odds ratio, 1.38; P = .02), over an average follow-up of 13 years, and this association was mediated by stress in 32% of cases. Emotional eating also was positively linked with a higher carotid-femoral pulse-wave velocity (cfPWV-beta), indicative of increased arterial stiffness. However, none of the three dimensions of eating behavior was associated with cardiovascular damage among the adolescents. In addition, none of the eating-behavior dimensions was tied to metabolic syndrome in the adult group (this association was not measured in the adolescents).
Energy intake had no apparent impact on any associations between eating behavior and CVD measures, Dr. Girerd said in the press release. “We might expect that emotional eaters would consume high-calorie foods, which would in turn lead to cardiovascular problems, but this was not the case. One explanation is that we measured average calorie intake and emotional eaters may binge when stressed and then eat less at other times,” and that the resulting “yo-yo” pattern might negatively affect the heart and blood vessels more than stable food intake, he said.
The study findings were limited by several factors, including the observational design that prevented conclusions of causality, the researchers noted. Other limitations included the use of a nonvalidated scale to measure stress, the lack of data on physical activity, and the use of a mainly healthy population in a limited geographic area, which may limit generalizability, they said.
More research is needed in other contexts and larger cohorts, but the results were strengthened by the large study population and the complete data on eating behaviors and detailed health information, they wrote. The results support previous studies and suggest that patients with emotional eating behavior could benefit from emotion regulation skills training, including cognitive, behavioral, psychological, and interpersonal therapies used in other areas, and from pharmacological treatments, the researchers concluded.
The current study offers a unique and important perspective on the relationship between diet and cardiovascular disease, Dr. Gulati, director of preventive cardiology at the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, told this news organization.
“Examining eating behavior and its relationship with cardiovascular effects in healthy individuals in this prospective way is quite interesting,” said Dr. Gulati, who was not involved in the study.
The researchers examined healthy people at baseline, inquired about their eating habits, and found that emotional eaters “have evidence of cardiovascular changes when compared with the other groups of eaters, after controlling for other risk factors that are associated with cardiovascular disease when following them for 13 years,” said Dr. Gulati, who was recently named Anita Dann Friedman Endowed Chair in Women’s Cardiovascular Medicine and Research at Cedars-Sinai. “This same finding wasn’t seen in adolescents, but this is probably because they are younger, and the effects aren’t seen. That is reassuring, because it means that the more we address eating behaviors, the more likely we are to reduce their effects to the heart,” she noted.
“This study is important because usually, as cardiologists or anyone in medicine, how we assess diet is by assessment of what food people eat; we don’t usually ask about what triggers them to eat,” Dr. Gulati said. “Eating behaviors based on their triggers ultimately affect food choice and food quantity, and help us understand weight changes during a lifetime,” she said.
“I think we don’t have the data to know that an eating behavior would be able to affect cardiac function,” said Dr. Gulati, “but I think we all might hypothesize that emotional eating may be associated with abnormal diastolic function simply through eating high-density food and weight gain.”
The current study did not show a relationship between eating behavior and metabolic syndrome, in contrast with prior studies, Dr. Gulati noted. However, “the authors report that the association between eating behaviors and diastolic dysfunction was mediated through the stress level,” Dr. Gulati said. “It is important to note that this European population was healthy at baseline, and also relatively healthy 13 years later, which makes these findings even more profound.”
Dr. Gulati said that she agrees with the study authors on the need to assess diet and eating behaviors when assessing cardiovascular risk in patient. “Diet assessment as part of prevention is central, but we should ask not only ‘what do you eat,’ but also ‘what makes you eat,’ ” she said.
More research is needed in other populations, Dr. Gulati added. The current study population was healthy at baseline and follow-up. Studies are needed in cohorts in the United States and in the developing world to see how the results might differ; as well as in rural America or in “food deserts” where food choices are limited.
Another research topic is the interplay between eating behaviors and social determinants of health, in terms of their effect on cardiovascular function, Dr. Gulati said, “and it will be valuable to follow this cohort further to see how these eating behaviors and these intermediate measures translate into cardiovascular outcomes.” Future studies should also examine whether the changes in cardiac function are reversible by interventions to modify eating behavior, particularly emotional eating, she said.
Supporters of the study included the Regional University Hospital Center of Nancy, the French Ministry of Solidarity and Health, and a public grant overseen by the French National Research Agency. The researchers had no financial conflicts to disclose.
Dr. Gulati, who serves on the editorial advisory board of MDedge Cardiology, had no financial conflicts to disclose.
Eating in response to stress – known as emotional eating – was significantly associated with several markers of long-term cardiovascular damage, based on data from 1,109 individuals.
“We know diet plays a huge role in cardiovascular disease, but we have focused a lot of work on what you eat, not on what makes you eat” – the current study did exactly that, Martha Gulati, MD, who wasn’t involved in the study, said in an interview.
“Emotional eaters consume food to satisfy their brains rather than their stomachs,” study investigator Nicolas Girerd, MD, of the National Institute of Health and Medical Research (INSERM) and a cardiologist at the University Hospital of Nancy (France), wrote in a press release accompanying the study.
Diet plays a role in the development of cardiovascular disease (CVD), but the impact of eating behavior on long-term cardiovascular health remains unclear, wrote Dr. Girerd and colleagues. Previous research has yielded three common psychological dimensions for eating behavior: emotional eating, restrained eating, and external eating.
Both emotional eating and restrained eating have been linked to cardiovascular disease risk, the researchers noted. “Because of previous findings, we hypothesized that [emotional and/or restrained dimensions of eating behavior] are positively associated with cardiovascular damages, as well as with CV risk factors, such as metabolic syndrome,” they wrote.
In a study published in the European Journal of Preventive Cardiology, the researchers reviewed data from 916 adults and 193 adolescents who were participants in the STANISLAS (Suivi Temporaire Annuel Non-Invasif de la Santé des Lorrains Assurés Sociaux), a longitudinal familial cohort in France. Cardiovascular data were collected at four medical visits as part of a full clinical examination between 1993 and 2016, with one visit every 5-10 years. Roughly one-third (31.0%) of the adults were overweight, 7.9% were obese, and 2.7% were underweight. The median age of the adults at the second visit was 44.7 years; the median age of the adolescent group was 15.2 years.
The primary outcome of cardiovascular damage was measured at the fourth visit. Eating behavior was assessed during the second visit using the Dutch Eating Behaviour Questionnaire (DEBQ), and participants were identified as emotional eaters, restrained eaters, or external eaters.
Among the adults, emotional eating was associated with a 38% increased risk of diastolic dysfunction (odds ratio, 1.38; P = .02), over an average follow-up of 13 years, and this association was mediated by stress in 32% of cases. Emotional eating also was positively linked with a higher carotid-femoral pulse-wave velocity (cfPWV-beta), indicative of increased arterial stiffness. However, none of the three dimensions of eating behavior was associated with cardiovascular damage among the adolescents. In addition, none of the eating-behavior dimensions was tied to metabolic syndrome in the adult group (this association was not measured in the adolescents).
Energy intake had no apparent impact on any associations between eating behavior and CVD measures, Dr. Girerd said in the press release. “We might expect that emotional eaters would consume high-calorie foods, which would in turn lead to cardiovascular problems, but this was not the case. One explanation is that we measured average calorie intake and emotional eaters may binge when stressed and then eat less at other times,” and that the resulting “yo-yo” pattern might negatively affect the heart and blood vessels more than stable food intake, he said.
The study findings were limited by several factors, including the observational design that prevented conclusions of causality, the researchers noted. Other limitations included the use of a nonvalidated scale to measure stress, the lack of data on physical activity, and the use of a mainly healthy population in a limited geographic area, which may limit generalizability, they said.
More research is needed in other contexts and larger cohorts, but the results were strengthened by the large study population and the complete data on eating behaviors and detailed health information, they wrote. The results support previous studies and suggest that patients with emotional eating behavior could benefit from emotion regulation skills training, including cognitive, behavioral, psychological, and interpersonal therapies used in other areas, and from pharmacological treatments, the researchers concluded.
The current study offers a unique and important perspective on the relationship between diet and cardiovascular disease, Dr. Gulati, director of preventive cardiology at the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, told this news organization.
“Examining eating behavior and its relationship with cardiovascular effects in healthy individuals in this prospective way is quite interesting,” said Dr. Gulati, who was not involved in the study.
The researchers examined healthy people at baseline, inquired about their eating habits, and found that emotional eaters “have evidence of cardiovascular changes when compared with the other groups of eaters, after controlling for other risk factors that are associated with cardiovascular disease when following them for 13 years,” said Dr. Gulati, who was recently named Anita Dann Friedman Endowed Chair in Women’s Cardiovascular Medicine and Research at Cedars-Sinai. “This same finding wasn’t seen in adolescents, but this is probably because they are younger, and the effects aren’t seen. That is reassuring, because it means that the more we address eating behaviors, the more likely we are to reduce their effects to the heart,” she noted.
“This study is important because usually, as cardiologists or anyone in medicine, how we assess diet is by assessment of what food people eat; we don’t usually ask about what triggers them to eat,” Dr. Gulati said. “Eating behaviors based on their triggers ultimately affect food choice and food quantity, and help us understand weight changes during a lifetime,” she said.
“I think we don’t have the data to know that an eating behavior would be able to affect cardiac function,” said Dr. Gulati, “but I think we all might hypothesize that emotional eating may be associated with abnormal diastolic function simply through eating high-density food and weight gain.”
The current study did not show a relationship between eating behavior and metabolic syndrome, in contrast with prior studies, Dr. Gulati noted. However, “the authors report that the association between eating behaviors and diastolic dysfunction was mediated through the stress level,” Dr. Gulati said. “It is important to note that this European population was healthy at baseline, and also relatively healthy 13 years later, which makes these findings even more profound.”
Dr. Gulati said that she agrees with the study authors on the need to assess diet and eating behaviors when assessing cardiovascular risk in patient. “Diet assessment as part of prevention is central, but we should ask not only ‘what do you eat,’ but also ‘what makes you eat,’ ” she said.
More research is needed in other populations, Dr. Gulati added. The current study population was healthy at baseline and follow-up. Studies are needed in cohorts in the United States and in the developing world to see how the results might differ; as well as in rural America or in “food deserts” where food choices are limited.
Another research topic is the interplay between eating behaviors and social determinants of health, in terms of their effect on cardiovascular function, Dr. Gulati said, “and it will be valuable to follow this cohort further to see how these eating behaviors and these intermediate measures translate into cardiovascular outcomes.” Future studies should also examine whether the changes in cardiac function are reversible by interventions to modify eating behavior, particularly emotional eating, she said.
Supporters of the study included the Regional University Hospital Center of Nancy, the French Ministry of Solidarity and Health, and a public grant overseen by the French National Research Agency. The researchers had no financial conflicts to disclose.
Dr. Gulati, who serves on the editorial advisory board of MDedge Cardiology, had no financial conflicts to disclose.
Eating in response to stress – known as emotional eating – was significantly associated with several markers of long-term cardiovascular damage, based on data from 1,109 individuals.
“We know diet plays a huge role in cardiovascular disease, but we have focused a lot of work on what you eat, not on what makes you eat” – the current study did exactly that, Martha Gulati, MD, who wasn’t involved in the study, said in an interview.
“Emotional eaters consume food to satisfy their brains rather than their stomachs,” study investigator Nicolas Girerd, MD, of the National Institute of Health and Medical Research (INSERM) and a cardiologist at the University Hospital of Nancy (France), wrote in a press release accompanying the study.
Diet plays a role in the development of cardiovascular disease (CVD), but the impact of eating behavior on long-term cardiovascular health remains unclear, wrote Dr. Girerd and colleagues. Previous research has yielded three common psychological dimensions for eating behavior: emotional eating, restrained eating, and external eating.
Both emotional eating and restrained eating have been linked to cardiovascular disease risk, the researchers noted. “Because of previous findings, we hypothesized that [emotional and/or restrained dimensions of eating behavior] are positively associated with cardiovascular damages, as well as with CV risk factors, such as metabolic syndrome,” they wrote.
In a study published in the European Journal of Preventive Cardiology, the researchers reviewed data from 916 adults and 193 adolescents who were participants in the STANISLAS (Suivi Temporaire Annuel Non-Invasif de la Santé des Lorrains Assurés Sociaux), a longitudinal familial cohort in France. Cardiovascular data were collected at four medical visits as part of a full clinical examination between 1993 and 2016, with one visit every 5-10 years. Roughly one-third (31.0%) of the adults were overweight, 7.9% were obese, and 2.7% were underweight. The median age of the adults at the second visit was 44.7 years; the median age of the adolescent group was 15.2 years.
The primary outcome of cardiovascular damage was measured at the fourth visit. Eating behavior was assessed during the second visit using the Dutch Eating Behaviour Questionnaire (DEBQ), and participants were identified as emotional eaters, restrained eaters, or external eaters.
Among the adults, emotional eating was associated with a 38% increased risk of diastolic dysfunction (odds ratio, 1.38; P = .02), over an average follow-up of 13 years, and this association was mediated by stress in 32% of cases. Emotional eating also was positively linked with a higher carotid-femoral pulse-wave velocity (cfPWV-beta), indicative of increased arterial stiffness. However, none of the three dimensions of eating behavior was associated with cardiovascular damage among the adolescents. In addition, none of the eating-behavior dimensions was tied to metabolic syndrome in the adult group (this association was not measured in the adolescents).
Energy intake had no apparent impact on any associations between eating behavior and CVD measures, Dr. Girerd said in the press release. “We might expect that emotional eaters would consume high-calorie foods, which would in turn lead to cardiovascular problems, but this was not the case. One explanation is that we measured average calorie intake and emotional eaters may binge when stressed and then eat less at other times,” and that the resulting “yo-yo” pattern might negatively affect the heart and blood vessels more than stable food intake, he said.
The study findings were limited by several factors, including the observational design that prevented conclusions of causality, the researchers noted. Other limitations included the use of a nonvalidated scale to measure stress, the lack of data on physical activity, and the use of a mainly healthy population in a limited geographic area, which may limit generalizability, they said.
More research is needed in other contexts and larger cohorts, but the results were strengthened by the large study population and the complete data on eating behaviors and detailed health information, they wrote. The results support previous studies and suggest that patients with emotional eating behavior could benefit from emotion regulation skills training, including cognitive, behavioral, psychological, and interpersonal therapies used in other areas, and from pharmacological treatments, the researchers concluded.
The current study offers a unique and important perspective on the relationship between diet and cardiovascular disease, Dr. Gulati, director of preventive cardiology at the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, told this news organization.
“Examining eating behavior and its relationship with cardiovascular effects in healthy individuals in this prospective way is quite interesting,” said Dr. Gulati, who was not involved in the study.
The researchers examined healthy people at baseline, inquired about their eating habits, and found that emotional eaters “have evidence of cardiovascular changes when compared with the other groups of eaters, after controlling for other risk factors that are associated with cardiovascular disease when following them for 13 years,” said Dr. Gulati, who was recently named Anita Dann Friedman Endowed Chair in Women’s Cardiovascular Medicine and Research at Cedars-Sinai. “This same finding wasn’t seen in adolescents, but this is probably because they are younger, and the effects aren’t seen. That is reassuring, because it means that the more we address eating behaviors, the more likely we are to reduce their effects to the heart,” she noted.
“This study is important because usually, as cardiologists or anyone in medicine, how we assess diet is by assessment of what food people eat; we don’t usually ask about what triggers them to eat,” Dr. Gulati said. “Eating behaviors based on their triggers ultimately affect food choice and food quantity, and help us understand weight changes during a lifetime,” she said.
“I think we don’t have the data to know that an eating behavior would be able to affect cardiac function,” said Dr. Gulati, “but I think we all might hypothesize that emotional eating may be associated with abnormal diastolic function simply through eating high-density food and weight gain.”
The current study did not show a relationship between eating behavior and metabolic syndrome, in contrast with prior studies, Dr. Gulati noted. However, “the authors report that the association between eating behaviors and diastolic dysfunction was mediated through the stress level,” Dr. Gulati said. “It is important to note that this European population was healthy at baseline, and also relatively healthy 13 years later, which makes these findings even more profound.”
Dr. Gulati said that she agrees with the study authors on the need to assess diet and eating behaviors when assessing cardiovascular risk in patient. “Diet assessment as part of prevention is central, but we should ask not only ‘what do you eat,’ but also ‘what makes you eat,’ ” she said.
More research is needed in other populations, Dr. Gulati added. The current study population was healthy at baseline and follow-up. Studies are needed in cohorts in the United States and in the developing world to see how the results might differ; as well as in rural America or in “food deserts” where food choices are limited.
Another research topic is the interplay between eating behaviors and social determinants of health, in terms of their effect on cardiovascular function, Dr. Gulati said, “and it will be valuable to follow this cohort further to see how these eating behaviors and these intermediate measures translate into cardiovascular outcomes.” Future studies should also examine whether the changes in cardiac function are reversible by interventions to modify eating behavior, particularly emotional eating, she said.
Supporters of the study included the Regional University Hospital Center of Nancy, the French Ministry of Solidarity and Health, and a public grant overseen by the French National Research Agency. The researchers had no financial conflicts to disclose.
Dr. Gulati, who serves on the editorial advisory board of MDedge Cardiology, had no financial conflicts to disclose.
FROM THE EUROPEAN JOURNAL OF PREVENTIVE CARDIOLOGY
Simulation-based training effective for transesophageal echo
Simulation-based teaching of transesophageal echocardiography (TEE) improved cardiology fellows’ knowledge, skills, and comfort with the procedure, compared with traditional training, a new study shows.
“TEE learning may be hampered by the lack of availability of teachers and equipment and by the need for esophageal intubation, which is semi-invasive,” Augustin Coisne, MD, PhD, of the Cardiovascular Research Foundation in New York, said in an interview. “In this setting, simulation emerges as a key educational tool, but we were lacking evidence supporting simulation-based educational programs.”
Fellows in the simulation group achieved higher theoretical test scores and practical test scores after the training than did those in the traditional group.
Furthermore, Dr. Coisne said, “the results of the subgroup analyses were surprising and unexpected. The effect of the simulation-based training was greater among fellows at the beginning of fellowship – i.e., 2 years or less of training – in both theoretical and practical tests and in women [versus men] for the theoretical test.”
Their results, from the randomized SIMULATOR study, were published online in JAMA Cardiology.
More ready, more confident
The researchers randomly assigned 324 cardiology fellows (mean age, 26.4 years; about 30% women) inexperienced in TEE from 42 French university centers to TEE training with or without simulation support. Both groups participated in traditional didactic training using e-learning with an online course that is compulsory for all cardiology fellows in France.
The simulation group also participated in two 2-hour teaching sessions using a TEE simulator.
Each fellow completed a theoretical and a practical test prior to training to assess their baseline TEE level and again 3 months after the end of the training program. A TEE simulator (U/S Mentor Simulator; 3D Systems Simbionix) was used for all tests, and 24 certified echocardiography teachers served as both trainers and raters.
The theoretical tests included 20 online video-based questions to evaluate recognition of standard TEE views, normal anatomy, and some pathological cases. Fellows had 90 seconds to choose the best answer for each question from five multiple-choice options.
For the practical tests, fellows had 3 minutes to familiarize themselves with the handling of the simulator, without specific training and before the probe introduction.
They were asked to show 10 basic views on the simulator and had a maximum of 1 minute for each view.
The coprimary outcomes were the scores in the final theoretical and practical tests. TEE duration and the fellows’ self-assessment of their proficiency were also evaluated.
At baseline, the theoretical and practical test scores were similar between the groups (33.0 for the simulator group vs. 32.5 for the traditional group, and 44.2 vs. 46.1, respectively).
After training, the fellows in the simulation group had higher theoretical and practical test scores than those in the traditional group (47.2% vs. 38.3% and 74.5% vs. 59.0%, respectively).
Score changes were consistently higher when the pretraining scores were lower, an association that was stronger in the simulation group.
Dr. Coisne noted that subgroup analyses showed that the effectiveness of the simulation training was greater when performed at the beginning of the fellowship. On the theoretical test, the point increase was 11.9 for the simulation group versus 4.25 points for the traditional training group; for the practical test, the increases were 24.0 points versus 10.1 points.
After training, it took significantly less time for the simulation group to complete a TEE than it did the traditional group (8.3 vs. 9.4 minutes).
Furthermore, simulation group fellows reported that they felt more ready (mean score, 3.0 vs. 1.7) and more confident (mean score, 3.3 vs. 2.4) about performing a TEE alone after training.
“The simulation approach is definitively scalable to every institution,” Dr. Coisne said. “However, a medico-economic analysis should be interesting because the cost of the simulator and its maintenance might be a limitation to spread simulation-based teaching. The possibility for smaller hospitals to pool their financial input to share a TEE simulator could be considered to increase its cost-effectiveness.”
Real-world outcomes required
Commenting on the study, S. Justin Szawlewicz, MD, chair of cardiovascular medicine at Deborah Heart and Lung Center in Brown Mills, N.J., pointed out that the authors indicated that the number of TEEs performed by the trainees was not collected.
“This would be useful information to determine if those who received simulator training sought out and performed more TEEs, and also to determine if cardiology trainees in France perform a similar number of TEEs as cardiology trainees in the United States.”
In addition, he said, “the 4 hours of simulator training in TEE is extra education and experience that the standard trainees didn’t get. Would 4 extra hours of standard training didactics also improve trainees’ scores?”
Noting that the fellows’ ability to perform TEE in real patients was not assessed, Dr. Szawlewicz said, “a study could be designed that evaluated TEE images from real patients to see if trainees receiving simulator training performed better, more comprehensive and efficient TEEs than standard training.”
Nevertheless, he concluded, “Four hours of simulator training appears to improve TEE knowledge and skills. This is something we would consider at our institution.”
Like Dr. Szawlewicz, Michael Spooner, MD, MBA, of Mercy One North Iowa Heart Center in Mason City, and Kathryn Bertlacher, MD, of the University of Pittsburgh Medical Center, noted in a related editorial, “data are not provided about change in the learner’s behavior or performance on an actual TEE after the course, nor are there data about clinical outcomes such as patient safety or completeness of subsequent TEEs.
“This limitation, which is a limitation of most of the existing TEE simulation literature, is a high bar to cross,” they concluded. “Reaching this bar will require studies such as this to provide foundational understanding.”
Twin-Medical provided the TEE simulators. No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
Simulation-based teaching of transesophageal echocardiography (TEE) improved cardiology fellows’ knowledge, skills, and comfort with the procedure, compared with traditional training, a new study shows.
“TEE learning may be hampered by the lack of availability of teachers and equipment and by the need for esophageal intubation, which is semi-invasive,” Augustin Coisne, MD, PhD, of the Cardiovascular Research Foundation in New York, said in an interview. “In this setting, simulation emerges as a key educational tool, but we were lacking evidence supporting simulation-based educational programs.”
Fellows in the simulation group achieved higher theoretical test scores and practical test scores after the training than did those in the traditional group.
Furthermore, Dr. Coisne said, “the results of the subgroup analyses were surprising and unexpected. The effect of the simulation-based training was greater among fellows at the beginning of fellowship – i.e., 2 years or less of training – in both theoretical and practical tests and in women [versus men] for the theoretical test.”
Their results, from the randomized SIMULATOR study, were published online in JAMA Cardiology.
More ready, more confident
The researchers randomly assigned 324 cardiology fellows (mean age, 26.4 years; about 30% women) inexperienced in TEE from 42 French university centers to TEE training with or without simulation support. Both groups participated in traditional didactic training using e-learning with an online course that is compulsory for all cardiology fellows in France.
The simulation group also participated in two 2-hour teaching sessions using a TEE simulator.
Each fellow completed a theoretical and a practical test prior to training to assess their baseline TEE level and again 3 months after the end of the training program. A TEE simulator (U/S Mentor Simulator; 3D Systems Simbionix) was used for all tests, and 24 certified echocardiography teachers served as both trainers and raters.
The theoretical tests included 20 online video-based questions to evaluate recognition of standard TEE views, normal anatomy, and some pathological cases. Fellows had 90 seconds to choose the best answer for each question from five multiple-choice options.
For the practical tests, fellows had 3 minutes to familiarize themselves with the handling of the simulator, without specific training and before the probe introduction.
They were asked to show 10 basic views on the simulator and had a maximum of 1 minute for each view.
The coprimary outcomes were the scores in the final theoretical and practical tests. TEE duration and the fellows’ self-assessment of their proficiency were also evaluated.
At baseline, the theoretical and practical test scores were similar between the groups (33.0 for the simulator group vs. 32.5 for the traditional group, and 44.2 vs. 46.1, respectively).
After training, the fellows in the simulation group had higher theoretical and practical test scores than those in the traditional group (47.2% vs. 38.3% and 74.5% vs. 59.0%, respectively).
Score changes were consistently higher when the pretraining scores were lower, an association that was stronger in the simulation group.
Dr. Coisne noted that subgroup analyses showed that the effectiveness of the simulation training was greater when performed at the beginning of the fellowship. On the theoretical test, the point increase was 11.9 for the simulation group versus 4.25 points for the traditional training group; for the practical test, the increases were 24.0 points versus 10.1 points.
After training, it took significantly less time for the simulation group to complete a TEE than it did the traditional group (8.3 vs. 9.4 minutes).
Furthermore, simulation group fellows reported that they felt more ready (mean score, 3.0 vs. 1.7) and more confident (mean score, 3.3 vs. 2.4) about performing a TEE alone after training.
“The simulation approach is definitively scalable to every institution,” Dr. Coisne said. “However, a medico-economic analysis should be interesting because the cost of the simulator and its maintenance might be a limitation to spread simulation-based teaching. The possibility for smaller hospitals to pool their financial input to share a TEE simulator could be considered to increase its cost-effectiveness.”
Real-world outcomes required
Commenting on the study, S. Justin Szawlewicz, MD, chair of cardiovascular medicine at Deborah Heart and Lung Center in Brown Mills, N.J., pointed out that the authors indicated that the number of TEEs performed by the trainees was not collected.
“This would be useful information to determine if those who received simulator training sought out and performed more TEEs, and also to determine if cardiology trainees in France perform a similar number of TEEs as cardiology trainees in the United States.”
In addition, he said, “the 4 hours of simulator training in TEE is extra education and experience that the standard trainees didn’t get. Would 4 extra hours of standard training didactics also improve trainees’ scores?”
Noting that the fellows’ ability to perform TEE in real patients was not assessed, Dr. Szawlewicz said, “a study could be designed that evaluated TEE images from real patients to see if trainees receiving simulator training performed better, more comprehensive and efficient TEEs than standard training.”
Nevertheless, he concluded, “Four hours of simulator training appears to improve TEE knowledge and skills. This is something we would consider at our institution.”
Like Dr. Szawlewicz, Michael Spooner, MD, MBA, of Mercy One North Iowa Heart Center in Mason City, and Kathryn Bertlacher, MD, of the University of Pittsburgh Medical Center, noted in a related editorial, “data are not provided about change in the learner’s behavior or performance on an actual TEE after the course, nor are there data about clinical outcomes such as patient safety or completeness of subsequent TEEs.
“This limitation, which is a limitation of most of the existing TEE simulation literature, is a high bar to cross,” they concluded. “Reaching this bar will require studies such as this to provide foundational understanding.”
Twin-Medical provided the TEE simulators. No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
Simulation-based teaching of transesophageal echocardiography (TEE) improved cardiology fellows’ knowledge, skills, and comfort with the procedure, compared with traditional training, a new study shows.
“TEE learning may be hampered by the lack of availability of teachers and equipment and by the need for esophageal intubation, which is semi-invasive,” Augustin Coisne, MD, PhD, of the Cardiovascular Research Foundation in New York, said in an interview. “In this setting, simulation emerges as a key educational tool, but we were lacking evidence supporting simulation-based educational programs.”
Fellows in the simulation group achieved higher theoretical test scores and practical test scores after the training than did those in the traditional group.
Furthermore, Dr. Coisne said, “the results of the subgroup analyses were surprising and unexpected. The effect of the simulation-based training was greater among fellows at the beginning of fellowship – i.e., 2 years or less of training – in both theoretical and practical tests and in women [versus men] for the theoretical test.”
Their results, from the randomized SIMULATOR study, were published online in JAMA Cardiology.
More ready, more confident
The researchers randomly assigned 324 cardiology fellows (mean age, 26.4 years; about 30% women) inexperienced in TEE from 42 French university centers to TEE training with or without simulation support. Both groups participated in traditional didactic training using e-learning with an online course that is compulsory for all cardiology fellows in France.
The simulation group also participated in two 2-hour teaching sessions using a TEE simulator.
Each fellow completed a theoretical and a practical test prior to training to assess their baseline TEE level and again 3 months after the end of the training program. A TEE simulator (U/S Mentor Simulator; 3D Systems Simbionix) was used for all tests, and 24 certified echocardiography teachers served as both trainers and raters.
The theoretical tests included 20 online video-based questions to evaluate recognition of standard TEE views, normal anatomy, and some pathological cases. Fellows had 90 seconds to choose the best answer for each question from five multiple-choice options.
For the practical tests, fellows had 3 minutes to familiarize themselves with the handling of the simulator, without specific training and before the probe introduction.
They were asked to show 10 basic views on the simulator and had a maximum of 1 minute for each view.
The coprimary outcomes were the scores in the final theoretical and practical tests. TEE duration and the fellows’ self-assessment of their proficiency were also evaluated.
At baseline, the theoretical and practical test scores were similar between the groups (33.0 for the simulator group vs. 32.5 for the traditional group, and 44.2 vs. 46.1, respectively).
After training, the fellows in the simulation group had higher theoretical and practical test scores than those in the traditional group (47.2% vs. 38.3% and 74.5% vs. 59.0%, respectively).
Score changes were consistently higher when the pretraining scores were lower, an association that was stronger in the simulation group.
Dr. Coisne noted that subgroup analyses showed that the effectiveness of the simulation training was greater when performed at the beginning of the fellowship. On the theoretical test, the point increase was 11.9 for the simulation group versus 4.25 points for the traditional training group; for the practical test, the increases were 24.0 points versus 10.1 points.
After training, it took significantly less time for the simulation group to complete a TEE than it did the traditional group (8.3 vs. 9.4 minutes).
Furthermore, simulation group fellows reported that they felt more ready (mean score, 3.0 vs. 1.7) and more confident (mean score, 3.3 vs. 2.4) about performing a TEE alone after training.
“The simulation approach is definitively scalable to every institution,” Dr. Coisne said. “However, a medico-economic analysis should be interesting because the cost of the simulator and its maintenance might be a limitation to spread simulation-based teaching. The possibility for smaller hospitals to pool their financial input to share a TEE simulator could be considered to increase its cost-effectiveness.”
Real-world outcomes required
Commenting on the study, S. Justin Szawlewicz, MD, chair of cardiovascular medicine at Deborah Heart and Lung Center in Brown Mills, N.J., pointed out that the authors indicated that the number of TEEs performed by the trainees was not collected.
“This would be useful information to determine if those who received simulator training sought out and performed more TEEs, and also to determine if cardiology trainees in France perform a similar number of TEEs as cardiology trainees in the United States.”
In addition, he said, “the 4 hours of simulator training in TEE is extra education and experience that the standard trainees didn’t get. Would 4 extra hours of standard training didactics also improve trainees’ scores?”
Noting that the fellows’ ability to perform TEE in real patients was not assessed, Dr. Szawlewicz said, “a study could be designed that evaluated TEE images from real patients to see if trainees receiving simulator training performed better, more comprehensive and efficient TEEs than standard training.”
Nevertheless, he concluded, “Four hours of simulator training appears to improve TEE knowledge and skills. This is something we would consider at our institution.”
Like Dr. Szawlewicz, Michael Spooner, MD, MBA, of Mercy One North Iowa Heart Center in Mason City, and Kathryn Bertlacher, MD, of the University of Pittsburgh Medical Center, noted in a related editorial, “data are not provided about change in the learner’s behavior or performance on an actual TEE after the course, nor are there data about clinical outcomes such as patient safety or completeness of subsequent TEEs.
“This limitation, which is a limitation of most of the existing TEE simulation literature, is a high bar to cross,” they concluded. “Reaching this bar will require studies such as this to provide foundational understanding.”
Twin-Medical provided the TEE simulators. No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
FROM JAMA CARDIOLOGY
Atrial failure or insufficiency: A new syndrome
Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.
“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.
The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
Pathology despite function
“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.
He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.
In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.
“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
New entity necessary?
Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.
One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.
“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.
Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.
The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.
For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”
“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.
“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.
Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.
A version of this article first appeared on Medscape.com.
Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.
“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.
The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
Pathology despite function
“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.
He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.
In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.
“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
New entity necessary?
Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.
One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.
“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.
Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.
The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.
For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”
“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.
“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.
Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.
A version of this article first appeared on Medscape.com.
Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.
“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.
The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
Pathology despite function
“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.
He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.
In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.
“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
New entity necessary?
Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.
One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.
“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.
Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.
The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.
For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”
“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.
“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.
Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.
A version of this article first appeared on Medscape.com.
PPI use in type 2 diabetes links with cardiovascular events
Among people with type 2 diabetes who self-reported regularly using a proton pump inhibitor (PPI), the incidence of cardiovascular disease (CVD) events as well as all-cause death was significantly increased in a study of more than 19,000 people with type 2 diabetes in a prospective U.K. database.
During median follow-up of about 11 years, regular use of a PPI by people with type 2 diabetes was significantly linked with a 27% relative increase in the incidence of coronary artery disease, compared with nonuse of a PPI, after full adjustment for potential confounding variables.
The results also show PPI use was significantly linked after full adjustment with a 34% relative increase in MI, a 35% relative increase in heart failure, and a 30% relative increase in all-cause death, say a team of Chinese researchers in a recent report in the Journal of Clinical Endocrinology and Metabolism.
PPIs are a medication class widely used in both over-the-counter and prescription formulations to reduce acid production in the stomach and to treat gastroesophageal reflux disease and other acid-related disorders. The PPI class includes such widely used agents as esomeprazole (Nexium), lansoprazole (Prevacid), and omeprazole (Prilosec).
The analyses in this report, which used data collected in the UK Biobank, are “rigorous,” and the findings of “a modest elevation of CVD risk are consistent with a growing number of observational studies in populations with and without diabetes,” commented Mary R. Rooney, PhD, an epidemiologist at Johns Hopkins University, Baltimore, who focuses on diabetes and cardiovascular diseases.
Prior observational reports
For example, a report from a prospective, observational study of more than 4300 U.S. residents published in 2021 that Dr. Rooney coauthored documented that cumulative PPI exposure for more than 5 years was significantly linked with a twofold increase in the rate of CVD events, compared with people who did not use a PPI. (This analysis did not examine a possible effect of diabetes status.)
And in a separate prospective, observational study of more than 1,000 Australians with type 2 diabetes, initiation of PPI treatment was significantly linked with a 3.6-fold increased incidence of CVD events, compared with PPI nonuse.
However, Dr. Rooney cautioned that the role of PPI use in raising CVD events “is still an unresolved question. It is too soon to tell if PPI use in people with diabetes should trigger additional caution.” Findings are needed from prospective, randomized trials to determine more definitively whether PPIs play a causal role in the incidence of CVD events, she said in an interview.
U.S. practice often results in unwarranted prolongation of PPI treatment, said the authors of an editorial that accompanied the 2021 report by Dr. Rooney and coauthors.
Long-term PPI use threatens harm
“The practice of initiating stress ulcer prophylaxis [by administering a PPI] in critical care is common,” wrote the authors of the 2021 editorial, Nitin Malik, MD, and William S. Weintraub, MD. “Although it is data driven and well intentioned, the possibility of causing harm – if it is continued on a long-term basis after resolution of the acute illness – is palpable.”
The new analyses using UK Biobank data included 19,229 adults with type 2 diabetes and no preexisting coronary artery disease, MI, heart failure, or stroke. The cohort included 15,954 people (83%) who did not report using a PPI and 3,275 who currently used PPIs regularly. Study limitations include self-report as the only verification of PPI use and lack of information on type of PPI, dose size, or use duration.
The findings remained consistent in several sensitivity analyses, including a propensity score–matched analysis and after further adjustment for use of histamine2 receptor antagonists, a drug class with indications similar to those for PPIs.
The authors of the report speculated that mechanisms that might link PPI use and increased CVD and mortality risk could include changes to the gut microbiota and possible interactions between PPIs and antiplatelet agents.
The study received no commercial funding. The authors and Dr. Rooney disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Among people with type 2 diabetes who self-reported regularly using a proton pump inhibitor (PPI), the incidence of cardiovascular disease (CVD) events as well as all-cause death was significantly increased in a study of more than 19,000 people with type 2 diabetes in a prospective U.K. database.
During median follow-up of about 11 years, regular use of a PPI by people with type 2 diabetes was significantly linked with a 27% relative increase in the incidence of coronary artery disease, compared with nonuse of a PPI, after full adjustment for potential confounding variables.
The results also show PPI use was significantly linked after full adjustment with a 34% relative increase in MI, a 35% relative increase in heart failure, and a 30% relative increase in all-cause death, say a team of Chinese researchers in a recent report in the Journal of Clinical Endocrinology and Metabolism.
PPIs are a medication class widely used in both over-the-counter and prescription formulations to reduce acid production in the stomach and to treat gastroesophageal reflux disease and other acid-related disorders. The PPI class includes such widely used agents as esomeprazole (Nexium), lansoprazole (Prevacid), and omeprazole (Prilosec).
The analyses in this report, which used data collected in the UK Biobank, are “rigorous,” and the findings of “a modest elevation of CVD risk are consistent with a growing number of observational studies in populations with and without diabetes,” commented Mary R. Rooney, PhD, an epidemiologist at Johns Hopkins University, Baltimore, who focuses on diabetes and cardiovascular diseases.
Prior observational reports
For example, a report from a prospective, observational study of more than 4300 U.S. residents published in 2021 that Dr. Rooney coauthored documented that cumulative PPI exposure for more than 5 years was significantly linked with a twofold increase in the rate of CVD events, compared with people who did not use a PPI. (This analysis did not examine a possible effect of diabetes status.)
And in a separate prospective, observational study of more than 1,000 Australians with type 2 diabetes, initiation of PPI treatment was significantly linked with a 3.6-fold increased incidence of CVD events, compared with PPI nonuse.
However, Dr. Rooney cautioned that the role of PPI use in raising CVD events “is still an unresolved question. It is too soon to tell if PPI use in people with diabetes should trigger additional caution.” Findings are needed from prospective, randomized trials to determine more definitively whether PPIs play a causal role in the incidence of CVD events, she said in an interview.
U.S. practice often results in unwarranted prolongation of PPI treatment, said the authors of an editorial that accompanied the 2021 report by Dr. Rooney and coauthors.
Long-term PPI use threatens harm
“The practice of initiating stress ulcer prophylaxis [by administering a PPI] in critical care is common,” wrote the authors of the 2021 editorial, Nitin Malik, MD, and William S. Weintraub, MD. “Although it is data driven and well intentioned, the possibility of causing harm – if it is continued on a long-term basis after resolution of the acute illness – is palpable.”
The new analyses using UK Biobank data included 19,229 adults with type 2 diabetes and no preexisting coronary artery disease, MI, heart failure, or stroke. The cohort included 15,954 people (83%) who did not report using a PPI and 3,275 who currently used PPIs regularly. Study limitations include self-report as the only verification of PPI use and lack of information on type of PPI, dose size, or use duration.
The findings remained consistent in several sensitivity analyses, including a propensity score–matched analysis and after further adjustment for use of histamine2 receptor antagonists, a drug class with indications similar to those for PPIs.
The authors of the report speculated that mechanisms that might link PPI use and increased CVD and mortality risk could include changes to the gut microbiota and possible interactions between PPIs and antiplatelet agents.
The study received no commercial funding. The authors and Dr. Rooney disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Among people with type 2 diabetes who self-reported regularly using a proton pump inhibitor (PPI), the incidence of cardiovascular disease (CVD) events as well as all-cause death was significantly increased in a study of more than 19,000 people with type 2 diabetes in a prospective U.K. database.
During median follow-up of about 11 years, regular use of a PPI by people with type 2 diabetes was significantly linked with a 27% relative increase in the incidence of coronary artery disease, compared with nonuse of a PPI, after full adjustment for potential confounding variables.
The results also show PPI use was significantly linked after full adjustment with a 34% relative increase in MI, a 35% relative increase in heart failure, and a 30% relative increase in all-cause death, say a team of Chinese researchers in a recent report in the Journal of Clinical Endocrinology and Metabolism.
PPIs are a medication class widely used in both over-the-counter and prescription formulations to reduce acid production in the stomach and to treat gastroesophageal reflux disease and other acid-related disorders. The PPI class includes such widely used agents as esomeprazole (Nexium), lansoprazole (Prevacid), and omeprazole (Prilosec).
The analyses in this report, which used data collected in the UK Biobank, are “rigorous,” and the findings of “a modest elevation of CVD risk are consistent with a growing number of observational studies in populations with and without diabetes,” commented Mary R. Rooney, PhD, an epidemiologist at Johns Hopkins University, Baltimore, who focuses on diabetes and cardiovascular diseases.
Prior observational reports
For example, a report from a prospective, observational study of more than 4300 U.S. residents published in 2021 that Dr. Rooney coauthored documented that cumulative PPI exposure for more than 5 years was significantly linked with a twofold increase in the rate of CVD events, compared with people who did not use a PPI. (This analysis did not examine a possible effect of diabetes status.)
And in a separate prospective, observational study of more than 1,000 Australians with type 2 diabetes, initiation of PPI treatment was significantly linked with a 3.6-fold increased incidence of CVD events, compared with PPI nonuse.
However, Dr. Rooney cautioned that the role of PPI use in raising CVD events “is still an unresolved question. It is too soon to tell if PPI use in people with diabetes should trigger additional caution.” Findings are needed from prospective, randomized trials to determine more definitively whether PPIs play a causal role in the incidence of CVD events, she said in an interview.
U.S. practice often results in unwarranted prolongation of PPI treatment, said the authors of an editorial that accompanied the 2021 report by Dr. Rooney and coauthors.
Long-term PPI use threatens harm
“The practice of initiating stress ulcer prophylaxis [by administering a PPI] in critical care is common,” wrote the authors of the 2021 editorial, Nitin Malik, MD, and William S. Weintraub, MD. “Although it is data driven and well intentioned, the possibility of causing harm – if it is continued on a long-term basis after resolution of the acute illness – is palpable.”
The new analyses using UK Biobank data included 19,229 adults with type 2 diabetes and no preexisting coronary artery disease, MI, heart failure, or stroke. The cohort included 15,954 people (83%) who did not report using a PPI and 3,275 who currently used PPIs regularly. Study limitations include self-report as the only verification of PPI use and lack of information on type of PPI, dose size, or use duration.
The findings remained consistent in several sensitivity analyses, including a propensity score–matched analysis and after further adjustment for use of histamine2 receptor antagonists, a drug class with indications similar to those for PPIs.
The authors of the report speculated that mechanisms that might link PPI use and increased CVD and mortality risk could include changes to the gut microbiota and possible interactions between PPIs and antiplatelet agents.
The study received no commercial funding. The authors and Dr. Rooney disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
Frail ADHF patients benefit more from early rehab
Patients with acute decompensated heart failure who were frail at baseline improved more with targeted, early physical rehabilitation than those who were prefrail, a new analysis of the REHAB-HF study suggests.
“The robust response to the intervention by frail patients exceeded our expectations,” Gordon R. Reeves, MD, PT, of Novant Health Heart and Vascular Institute, Charlotte, N.C., told this news organization. “The effect size from improvement in physical function among frail patients was very large, with at least four times the minimal meaningful improvement, based on the Short Physical Performance Battery (SPPB).”
Furthermore, the interaction between baseline frailty status and treatment in REHAB-HF was such that a 2.6-fold larger improvement in SPPB was seen among frail versus prefrail patients.
However, Dr. Reeves noted, “We need to further evaluate safety and efficacy as it relates to adverse clinical events. Specifically, we observed a numerically higher number of deaths with the REHAB-HF intervention, which warrants further investigation before the intervention is implemented in clinical practice.”
The study was published online in JAMA Cardiology.
Interpret with caution
Dr. Reeves and colleagues conducted a prespecified secondary analysis of the previously published Therapy in Older Acute Heart Failure Patients (REHAB-HF) trial, a multicenter, randomized controlled trial that showed that a 3-month early, transitional, tailored, multidomain physical rehabilitation intervention improved physical function and quality of life (QoL), compared with usual care. The secondary analysis aimed to evaluate whether baseline frailty altered the benefits of the intervention or was associated with risk of adverse outcomes.
According to Dr. Reeves, REHAB-HF differs from more traditional cardiac rehab programs in several ways.
- The intervention targets patients with acute HF, including HF with preserved ejection fraction (HFpEF). Medicare policy limits standard cardiac rehabilitation in HF to long-term patients with HF with reduced ejection fraction (HFrEF) only who have been stabilized for 6 weeks or longer after a recent hospitalization.
- It addresses multiple physical function domains, including balance, mobility, functional strength, and endurance. Standard cardiac rehab is primarily focused on endurance training, which can result in injuries and falls if deficits in balance, mobility, and strength are not addressed first.
- It is delivered one to one rather than in a group setting and primarily by physical therapists who are experts in the rehabilitation of medically complex patients.
- It is transitional, beginning in the hospital, then moving to the outpatient setting, then to home and includes a home assessment.
For the analysis, the Fried phenotype model was used to assess baseline frailty across five domains: unintentional weight loss during the past year; self-reported exhaustion; grip strength; slowness, as assessed by gait speed; and low physical activity, as assessed by the Short Form-12 Physical Composite Score.
At the baseline visit, patients were categorized as frail if they met three or more of these criteria. They were categorized as prefrail if they met one or two criteria and as nonfrail if they met none of the criteria. Because of the small number of nonfrail participants, the analysis included only frail and prefrail participants.
The analysis included 337 participants (mean age, 72; 54%, women; 50%, Black). At baseline, 57% were frail, and 43% were prefrail.
A significant interaction was seen between baseline frailty and the intervention for the primary trial endpoint of overall SPPB score, with a 2.6-fold larger improvement in SPPB among frail (2.1) versus prefrail (0.8) patients.
Trends favored a larger intervention effect size, with significant improvement among frail versus prefrail participants for 6-minute walk distance, QoL, and the geriatric depression score.
“However, we must interpret these findings with caution,” the authors write. “The REHAB-HF trial was not adequately powered to determine the effect of the intervention on clinical events.” This plus the number of deaths “underscore the need for additional research, including prospective clinical trials, investigating the effect of physical function interventions on clinical events among frail patients with HF.”
To address this need, the researchers recently launched a larger clinical trial, called REHAB-HFpEF, which is powered to assess the impact of the intervention on clinical events, according to Dr. Reeves. “As the name implies,” he said, “this trial is focused on older patients recently hospitalized with HFpEF, who, [compared with HFrEF] also showed a more robust response to the intervention, with worse physical function and very high prevalence of frailty near the time of hospital discharge.”
‘Never too old or sick to benefit’
Jonathan H. Whiteson, MD, vice chair of clinical operations and medical director of cardiac and pulmonary rehabilitation at NYU Langone Health’s Rusk Rehabilitation, said, “We have seen in clinical practice and in other (non–heart failure) clinical areas that frail older patients do improve proportionally more than younger and less frail patients with rehabilitation programs. Encouragingly, this very much supports the practice that patients are never too old or too sick to benefit from an individualized multidisciplinary rehabilitation program.”
However, he noted, “patients had to be independent with basic activities of daily living to be included in the study,” so many frail, elderly patients with heart failure who are not independent were not included in the study. It also wasn’t clear whether patients who received postacute care at a rehab facility before going home were included in the trial.
Furthermore, he said, outcomes over 1 to 5 years are needed to understand the long-term impact of the intervention.
On the other hand, he added, the fact that about half of participants were Black and were women is a “tremendous strength.”
“Repeating this study in population groups at high risk for frailty with different diagnoses, such as chronic lung diseases, interstitial lung diseases, chronic kidney disease, and rheumatologic disorders will further support the value of rehabilitation in improving patient health, function, quality of life, and reducing rehospitalizations and health care costs,” Dr. Whiteson concluded.
The study was supported by grants from the National Key R&D program. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Patients with acute decompensated heart failure who were frail at baseline improved more with targeted, early physical rehabilitation than those who were prefrail, a new analysis of the REHAB-HF study suggests.
“The robust response to the intervention by frail patients exceeded our expectations,” Gordon R. Reeves, MD, PT, of Novant Health Heart and Vascular Institute, Charlotte, N.C., told this news organization. “The effect size from improvement in physical function among frail patients was very large, with at least four times the minimal meaningful improvement, based on the Short Physical Performance Battery (SPPB).”
Furthermore, the interaction between baseline frailty status and treatment in REHAB-HF was such that a 2.6-fold larger improvement in SPPB was seen among frail versus prefrail patients.
However, Dr. Reeves noted, “We need to further evaluate safety and efficacy as it relates to adverse clinical events. Specifically, we observed a numerically higher number of deaths with the REHAB-HF intervention, which warrants further investigation before the intervention is implemented in clinical practice.”
The study was published online in JAMA Cardiology.
Interpret with caution
Dr. Reeves and colleagues conducted a prespecified secondary analysis of the previously published Therapy in Older Acute Heart Failure Patients (REHAB-HF) trial, a multicenter, randomized controlled trial that showed that a 3-month early, transitional, tailored, multidomain physical rehabilitation intervention improved physical function and quality of life (QoL), compared with usual care. The secondary analysis aimed to evaluate whether baseline frailty altered the benefits of the intervention or was associated with risk of adverse outcomes.
According to Dr. Reeves, REHAB-HF differs from more traditional cardiac rehab programs in several ways.
- The intervention targets patients with acute HF, including HF with preserved ejection fraction (HFpEF). Medicare policy limits standard cardiac rehabilitation in HF to long-term patients with HF with reduced ejection fraction (HFrEF) only who have been stabilized for 6 weeks or longer after a recent hospitalization.
- It addresses multiple physical function domains, including balance, mobility, functional strength, and endurance. Standard cardiac rehab is primarily focused on endurance training, which can result in injuries and falls if deficits in balance, mobility, and strength are not addressed first.
- It is delivered one to one rather than in a group setting and primarily by physical therapists who are experts in the rehabilitation of medically complex patients.
- It is transitional, beginning in the hospital, then moving to the outpatient setting, then to home and includes a home assessment.
For the analysis, the Fried phenotype model was used to assess baseline frailty across five domains: unintentional weight loss during the past year; self-reported exhaustion; grip strength; slowness, as assessed by gait speed; and low physical activity, as assessed by the Short Form-12 Physical Composite Score.
At the baseline visit, patients were categorized as frail if they met three or more of these criteria. They were categorized as prefrail if they met one or two criteria and as nonfrail if they met none of the criteria. Because of the small number of nonfrail participants, the analysis included only frail and prefrail participants.
The analysis included 337 participants (mean age, 72; 54%, women; 50%, Black). At baseline, 57% were frail, and 43% were prefrail.
A significant interaction was seen between baseline frailty and the intervention for the primary trial endpoint of overall SPPB score, with a 2.6-fold larger improvement in SPPB among frail (2.1) versus prefrail (0.8) patients.
Trends favored a larger intervention effect size, with significant improvement among frail versus prefrail participants for 6-minute walk distance, QoL, and the geriatric depression score.
“However, we must interpret these findings with caution,” the authors write. “The REHAB-HF trial was not adequately powered to determine the effect of the intervention on clinical events.” This plus the number of deaths “underscore the need for additional research, including prospective clinical trials, investigating the effect of physical function interventions on clinical events among frail patients with HF.”
To address this need, the researchers recently launched a larger clinical trial, called REHAB-HFpEF, which is powered to assess the impact of the intervention on clinical events, according to Dr. Reeves. “As the name implies,” he said, “this trial is focused on older patients recently hospitalized with HFpEF, who, [compared with HFrEF] also showed a more robust response to the intervention, with worse physical function and very high prevalence of frailty near the time of hospital discharge.”
‘Never too old or sick to benefit’
Jonathan H. Whiteson, MD, vice chair of clinical operations and medical director of cardiac and pulmonary rehabilitation at NYU Langone Health’s Rusk Rehabilitation, said, “We have seen in clinical practice and in other (non–heart failure) clinical areas that frail older patients do improve proportionally more than younger and less frail patients with rehabilitation programs. Encouragingly, this very much supports the practice that patients are never too old or too sick to benefit from an individualized multidisciplinary rehabilitation program.”
However, he noted, “patients had to be independent with basic activities of daily living to be included in the study,” so many frail, elderly patients with heart failure who are not independent were not included in the study. It also wasn’t clear whether patients who received postacute care at a rehab facility before going home were included in the trial.
Furthermore, he said, outcomes over 1 to 5 years are needed to understand the long-term impact of the intervention.
On the other hand, he added, the fact that about half of participants were Black and were women is a “tremendous strength.”
“Repeating this study in population groups at high risk for frailty with different diagnoses, such as chronic lung diseases, interstitial lung diseases, chronic kidney disease, and rheumatologic disorders will further support the value of rehabilitation in improving patient health, function, quality of life, and reducing rehospitalizations and health care costs,” Dr. Whiteson concluded.
The study was supported by grants from the National Key R&D program. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Patients with acute decompensated heart failure who were frail at baseline improved more with targeted, early physical rehabilitation than those who were prefrail, a new analysis of the REHAB-HF study suggests.
“The robust response to the intervention by frail patients exceeded our expectations,” Gordon R. Reeves, MD, PT, of Novant Health Heart and Vascular Institute, Charlotte, N.C., told this news organization. “The effect size from improvement in physical function among frail patients was very large, with at least four times the minimal meaningful improvement, based on the Short Physical Performance Battery (SPPB).”
Furthermore, the interaction between baseline frailty status and treatment in REHAB-HF was such that a 2.6-fold larger improvement in SPPB was seen among frail versus prefrail patients.
However, Dr. Reeves noted, “We need to further evaluate safety and efficacy as it relates to adverse clinical events. Specifically, we observed a numerically higher number of deaths with the REHAB-HF intervention, which warrants further investigation before the intervention is implemented in clinical practice.”
The study was published online in JAMA Cardiology.
Interpret with caution
Dr. Reeves and colleagues conducted a prespecified secondary analysis of the previously published Therapy in Older Acute Heart Failure Patients (REHAB-HF) trial, a multicenter, randomized controlled trial that showed that a 3-month early, transitional, tailored, multidomain physical rehabilitation intervention improved physical function and quality of life (QoL), compared with usual care. The secondary analysis aimed to evaluate whether baseline frailty altered the benefits of the intervention or was associated with risk of adverse outcomes.
According to Dr. Reeves, REHAB-HF differs from more traditional cardiac rehab programs in several ways.
- The intervention targets patients with acute HF, including HF with preserved ejection fraction (HFpEF). Medicare policy limits standard cardiac rehabilitation in HF to long-term patients with HF with reduced ejection fraction (HFrEF) only who have been stabilized for 6 weeks or longer after a recent hospitalization.
- It addresses multiple physical function domains, including balance, mobility, functional strength, and endurance. Standard cardiac rehab is primarily focused on endurance training, which can result in injuries and falls if deficits in balance, mobility, and strength are not addressed first.
- It is delivered one to one rather than in a group setting and primarily by physical therapists who are experts in the rehabilitation of medically complex patients.
- It is transitional, beginning in the hospital, then moving to the outpatient setting, then to home and includes a home assessment.
For the analysis, the Fried phenotype model was used to assess baseline frailty across five domains: unintentional weight loss during the past year; self-reported exhaustion; grip strength; slowness, as assessed by gait speed; and low physical activity, as assessed by the Short Form-12 Physical Composite Score.
At the baseline visit, patients were categorized as frail if they met three or more of these criteria. They were categorized as prefrail if they met one or two criteria and as nonfrail if they met none of the criteria. Because of the small number of nonfrail participants, the analysis included only frail and prefrail participants.
The analysis included 337 participants (mean age, 72; 54%, women; 50%, Black). At baseline, 57% were frail, and 43% were prefrail.
A significant interaction was seen between baseline frailty and the intervention for the primary trial endpoint of overall SPPB score, with a 2.6-fold larger improvement in SPPB among frail (2.1) versus prefrail (0.8) patients.
Trends favored a larger intervention effect size, with significant improvement among frail versus prefrail participants for 6-minute walk distance, QoL, and the geriatric depression score.
“However, we must interpret these findings with caution,” the authors write. “The REHAB-HF trial was not adequately powered to determine the effect of the intervention on clinical events.” This plus the number of deaths “underscore the need for additional research, including prospective clinical trials, investigating the effect of physical function interventions on clinical events among frail patients with HF.”
To address this need, the researchers recently launched a larger clinical trial, called REHAB-HFpEF, which is powered to assess the impact of the intervention on clinical events, according to Dr. Reeves. “As the name implies,” he said, “this trial is focused on older patients recently hospitalized with HFpEF, who, [compared with HFrEF] also showed a more robust response to the intervention, with worse physical function and very high prevalence of frailty near the time of hospital discharge.”
‘Never too old or sick to benefit’
Jonathan H. Whiteson, MD, vice chair of clinical operations and medical director of cardiac and pulmonary rehabilitation at NYU Langone Health’s Rusk Rehabilitation, said, “We have seen in clinical practice and in other (non–heart failure) clinical areas that frail older patients do improve proportionally more than younger and less frail patients with rehabilitation programs. Encouragingly, this very much supports the practice that patients are never too old or too sick to benefit from an individualized multidisciplinary rehabilitation program.”
However, he noted, “patients had to be independent with basic activities of daily living to be included in the study,” so many frail, elderly patients with heart failure who are not independent were not included in the study. It also wasn’t clear whether patients who received postacute care at a rehab facility before going home were included in the trial.
Furthermore, he said, outcomes over 1 to 5 years are needed to understand the long-term impact of the intervention.
On the other hand, he added, the fact that about half of participants were Black and were women is a “tremendous strength.”
“Repeating this study in population groups at high risk for frailty with different diagnoses, such as chronic lung diseases, interstitial lung diseases, chronic kidney disease, and rheumatologic disorders will further support the value of rehabilitation in improving patient health, function, quality of life, and reducing rehospitalizations and health care costs,” Dr. Whiteson concluded.
The study was supported by grants from the National Key R&D program. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Atrial fibrillation: Sex differences and modifiable risk factors
This transcript has been edited for clarity.
Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital.
We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.
As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.
It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.
AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.
It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.
We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital.
We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.
As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.
It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.
AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.
It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.
We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital.
We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.
As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.
It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.
AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.
It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.
We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.
A version of this article first appeared on Medscape.com.
Top cardiology societies call for revamp of clinical trials
Leading cardiology societies have issued a “call for action” on a global scale to reinvent randomized clinical trials fit for the 21st century.
“Randomized trials are an essential tool for reliably assessing the effects of treatments, but they have become too costly and too burdensome,” first author Louise Bowman, University of Oxford, England, told this news organization. “We urgently need to modernize our approach to clinical trials in order to continue to improve patient care.”
The joint opinion is from the European Society of Cardiology, the American Heart Association, the American College of Cardiology, and the World Heart Federation. It was simultaneously published online in the European Heart Journal, Circulation, Journal of the American College of Cardiology, and Global Heart.
The authors note that the availability of large-scale “real-world” data is increasingly being touted as a way to bypass the challenges of conducting randomized trials. Yet, observational analyses of real-world data “are not a suitable alternative to randomization,” Prof. Bowman said.
Cardiology has historically led the way in transforming clinical practice with groundbreaking “mega-trials,” such as the International Study of Infarct Survival (ISIS), Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto (GISSI), and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO).
But over the past 25 years, there has been a huge increase in the rules and related bureaucracy governing clinical trials, which hinders the ability to conduct trials swiftly and affordably, the authors point out.
The COVID-19 pandemic has shown that important clinical trials can be performed quickly and efficiently in busy hospitals, they note.
“The RECOVERY trial in COVID-19 has been an excellent example of this, with results that are estimated to have saved around 1 million lives worldwide within just 1 year,” Prof. Bowman told this news organization.
A Good Clinical Trials Collaborative made up of key stakeholders recently developed new guidelines designed to promote better, more efficient randomized controlled trials.
“If widely adopted and used alongside valuable 21st century electronic health records, we could transform the clinical trials landscape and do many more high-quality trials very cost-effectively,” Prof. Bowman said.
“Widespread adoption and implementation of the revised guidelines will require collaboration with a wide range of national and international organizations, including patient, professional, academic, and industry groups, funders and government organizations, and ethics, health policy, and regulatory bodies,” Prof. Bowman acknowledged.
“This is work that the Good Clinical Trials Collaborative is leading. It is hoped that this endorsement by the joint cardiovascular societies will increase awareness and provide valuable support to his important work,” she added.
No commercial funding was received. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Leading cardiology societies have issued a “call for action” on a global scale to reinvent randomized clinical trials fit for the 21st century.
“Randomized trials are an essential tool for reliably assessing the effects of treatments, but they have become too costly and too burdensome,” first author Louise Bowman, University of Oxford, England, told this news organization. “We urgently need to modernize our approach to clinical trials in order to continue to improve patient care.”
The joint opinion is from the European Society of Cardiology, the American Heart Association, the American College of Cardiology, and the World Heart Federation. It was simultaneously published online in the European Heart Journal, Circulation, Journal of the American College of Cardiology, and Global Heart.
The authors note that the availability of large-scale “real-world” data is increasingly being touted as a way to bypass the challenges of conducting randomized trials. Yet, observational analyses of real-world data “are not a suitable alternative to randomization,” Prof. Bowman said.
Cardiology has historically led the way in transforming clinical practice with groundbreaking “mega-trials,” such as the International Study of Infarct Survival (ISIS), Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto (GISSI), and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO).
But over the past 25 years, there has been a huge increase in the rules and related bureaucracy governing clinical trials, which hinders the ability to conduct trials swiftly and affordably, the authors point out.
The COVID-19 pandemic has shown that important clinical trials can be performed quickly and efficiently in busy hospitals, they note.
“The RECOVERY trial in COVID-19 has been an excellent example of this, with results that are estimated to have saved around 1 million lives worldwide within just 1 year,” Prof. Bowman told this news organization.
A Good Clinical Trials Collaborative made up of key stakeholders recently developed new guidelines designed to promote better, more efficient randomized controlled trials.
“If widely adopted and used alongside valuable 21st century electronic health records, we could transform the clinical trials landscape and do many more high-quality trials very cost-effectively,” Prof. Bowman said.
“Widespread adoption and implementation of the revised guidelines will require collaboration with a wide range of national and international organizations, including patient, professional, academic, and industry groups, funders and government organizations, and ethics, health policy, and regulatory bodies,” Prof. Bowman acknowledged.
“This is work that the Good Clinical Trials Collaborative is leading. It is hoped that this endorsement by the joint cardiovascular societies will increase awareness and provide valuable support to his important work,” she added.
No commercial funding was received. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Leading cardiology societies have issued a “call for action” on a global scale to reinvent randomized clinical trials fit for the 21st century.
“Randomized trials are an essential tool for reliably assessing the effects of treatments, but they have become too costly and too burdensome,” first author Louise Bowman, University of Oxford, England, told this news organization. “We urgently need to modernize our approach to clinical trials in order to continue to improve patient care.”
The joint opinion is from the European Society of Cardiology, the American Heart Association, the American College of Cardiology, and the World Heart Federation. It was simultaneously published online in the European Heart Journal, Circulation, Journal of the American College of Cardiology, and Global Heart.
The authors note that the availability of large-scale “real-world” data is increasingly being touted as a way to bypass the challenges of conducting randomized trials. Yet, observational analyses of real-world data “are not a suitable alternative to randomization,” Prof. Bowman said.
Cardiology has historically led the way in transforming clinical practice with groundbreaking “mega-trials,” such as the International Study of Infarct Survival (ISIS), Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto (GISSI), and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO).
But over the past 25 years, there has been a huge increase in the rules and related bureaucracy governing clinical trials, which hinders the ability to conduct trials swiftly and affordably, the authors point out.
The COVID-19 pandemic has shown that important clinical trials can be performed quickly and efficiently in busy hospitals, they note.
“The RECOVERY trial in COVID-19 has been an excellent example of this, with results that are estimated to have saved around 1 million lives worldwide within just 1 year,” Prof. Bowman told this news organization.
A Good Clinical Trials Collaborative made up of key stakeholders recently developed new guidelines designed to promote better, more efficient randomized controlled trials.
“If widely adopted and used alongside valuable 21st century electronic health records, we could transform the clinical trials landscape and do many more high-quality trials very cost-effectively,” Prof. Bowman said.
“Widespread adoption and implementation of the revised guidelines will require collaboration with a wide range of national and international organizations, including patient, professional, academic, and industry groups, funders and government organizations, and ethics, health policy, and regulatory bodies,” Prof. Bowman acknowledged.
“This is work that the Good Clinical Trials Collaborative is leading. It is hoped that this endorsement by the joint cardiovascular societies will increase awareness and provide valuable support to his important work,” she added.
No commercial funding was received. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Endocarditis tied to drug use on the rise, spiked during COVID
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A new study provides more evidence that endocarditis associated with drug use is a significant and growing health concern, and further demonstrates that this risk has been exacerbated by the COVID-19 pandemic.
The rate of infective endocarditis among individuals in the United States with opioid or cocaine use disorder increased in the 11-year period 2011 to 2022, with the steepest increase logged during the COVID-19 pandemic (2021-2022), according to the study.
A diagnosis of COVID-19 more than doubled the risk for a new diagnosis of endocarditis in patients with either cocaine (hazard ratio, 2.24) or opioid use disorder (HR, 2.23).
“Our data suggests that, in addition to the major social disruption from the pandemic, including disrupted access to health care, COVID-19 infection itself is a significant risk factor for new diagnosis of endocarditis in drug using populations,” authors Nora Volkow, MD, director of the National Institute on Drug Abuse, and colleagues wrote.
“Drug-using populations, particularly those who use cocaine or opioids, have some of the highest risk for endocarditis, and here we show that having a COVID-19 diagnoses further increases this risk,” they added.
The study was published online in Molecular Psychiatry.
The researchers analyzed electronic health record data collected from January 2011 to August 2022 for more than 109 million people across the United States, including more than 736,000 with an opioid use disorder and more than 379,000 with a cocaine use disorder.
In 2011, there were 4 cases of endocarditis per day for every 1 million people with opioid use disorder. By 2022, the rate had increased to 30 cases per day per 1 million people with opioid use disorder.
For people with cocaine use disorder, cases of endocarditis increased from 5 per 1 million in 2011 to 23 per 1 million in 2022.
Among individuals with cocaine or opioid use disorder, the risk of being hospitalized within 180 days following a diagnosis of endocarditis was higher in those with than without COVID-19 (67.5% vs. 58.7%; HR, 1.21).
The risk of dying within 180 days following new diagnosis of endocarditis was also higher in those with than without COVID-19 (9.2% vs. 8%; HR, 1.16).
The study also showed that Black and Hispanic individuals had a lower risk for COVID-19-associated endocarditis than non-Hispanic White individuals, which is consistent with a higher prevalence of injection drug use in non-Hispanic White populations, compared with Black or Hispanic populations, the researchers pointed out.
Dr. Volkow and colleagues said their findings highlight the need to screen drug users for endocarditis and link them to infectious disease and addiction treatment if they contract COVID-19.
“People with substance use disorder already face major impediments to proper health care due to lack of access and stigma,” Dr. Volkow said in a news release.
“Proven techniques like syringe service programs, which help people avoid infection from reused or shared injection equipment, can help prevent this often fatal and costly condition,” Dr. Volkow added.
The authors said it will also be important to determine exactly how SARS-CoV-2 viral infection exacerbates the risk for endocarditis in drug users.
Support for the study was provided by the National Institute on Aging, National Institute on Alcohol Abuse and Alcoholism, the Clinical and Translational Science Collaborative of Cleveland, and the National Cancer Institute Case Comprehensive Cancer Center. The authors reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM MOLECULAR PSYCHIATRY