You're listening to This Week in Cardiology from TheHeart.org, Medscape Cardiology. This podcast is intended for healthcare professionals only. Any views expressed are the presenter's own and do not necessarily reflect the views of WebMD or Medscape. Hi everyone, this is John Mandrola from TheHeart.org, Medscape Cardiology, and this is This Week in Cardiology for January 23rd, 2026. This week, I'll discuss the value of procedural volume for TAVR and mitral valve trans catheter edge-to-edge repair, ventricular arrhythmia in older athletes, and the Goldilocks time horizon for predicting and modifying cardiovascular risk. The first thing to say is that Louisville, Kentucky, my home, faces a snow apocalypse this weekend. They say it might be the biggest storm in the last 50 years to hit this area. And of course, we live in the southern part of the United States, and we are not used to snow here, so it could be interesting. The second thing to say is I have two listener feedbacks today. Dr. Jan Kleberger from Zurich writes about my coverage of the Withdraw AF trial last week, where patients with AFib-related left ventricular dysfunction were treated, and then the ejection fraction recovered, and then these patients were subsequently randomized to medication withdrawal or medication continuation. And withdrawal IAF was a really neat study because it had a crossover. Kleberg writes that a nuance that he would like to emphasize is terminology and underlying assumptions. He says that the concept of lone atrial fib remains controversial, is no longer supported by contemporary guidelines, largely because of the absence of detected disease, often reflects incomplete phenotyping rather than a distinct clinical entity. Closely related, he goes on to say, the notion of a specific AF-mediated cardiomyopathy is still hypothetical. While AF burden, tachycardia, and rhythm irregularity all may contribute to LV dysfunction in some patients, there is currently no definitive proof that this represents a distinct reversible cardiomyopathy rather than a manifestation of underlying myocardial vulnerability and arrhythmogenic substrate. And against that background, Kleberger worries that the trial is easy to over-extrapolate. Withdraw AF enrolled a small, highly selected population with recovered ejection fraction following rhythm control, but the mechanistic link between AF and the initial LV dysfunction remains inferential. The randomized sample size was limited and the follow-up after GDMT withdrawal was short on the order of months, and that constrains our ability to assess longer term relapse risk and myocardial remodeling trajectories. And so therefore, Dr. Kleberger's takeaway is that the trial supports feasibility of carefully monitored individualized GDMT withdrawal in select patients with a low threshold for rapid reinitiation. However, it does not yet provide sufficient evidence to justify routine withdrawal of heart failure therapies in these patients, particularly when the underlying pathophysiology is uncertain and long-term outcomes remain unknown. And I could not agree more. In fact, I am so happy that I receive listener feedback this good. I pulled this quote from my summary last week. I wrote that and said that I think this evidence provides at least reason to consider careful withdrawal in selected patients who want to reduce pill burden and are willing to have more active surveillance. So I think the emphasis here from Withdraw AF is highly selected patients, careful withdrawal, and active surveillance. The second listener feedback comment came from Dr. Douglas Rosing from the NIH, and it regarded my coverage of that amazing vector procedure. Rosing writes that I I rightly gave credit to the Emory team for achieving a successful percutaneous bypass procedure, but I failed to mention the concept behind Vector was developed by work at the cardiology branch of the NIH and was first tested there in an animal model. The first author of the paper I cited was Christopher Bruce when he was at NIH, and it was in the laboratory of Robert Lederman that the work occurred. Dr. Lederman is incredibly creative and has developed in his laboratory a number of first-in-man procedures, including Basilica, Sesame, Lampoon, Cathedral, Transcaval, Aortic Excess, etc. And Roasting writes that I am sure you did not intentionally omit the NIH and Drs. Liederman and Bruce. And no, I did not and I never intentionally leave out people. After a decade of doing this podcast, I still struggle to get the right balance between describing a study, appraising a study, and giving credit for specific work. And it's difficult for me because most often I'm reading a manuscript a lot of times in the area where I'm not an expert and I actually don't know the top labs or whatever in this area. I'm mostly just describing the procedure. So thanks for writing, Dr. Rosing. All right. First topic is procedural volume and outcomes for TAVI and mitral valve transcatheter edge to edge repair. JAMA Cardiology has published a classic observational study which looks at the association between an operator's and hospital's volume and their outcomes for TAVI and M-TIER. This is a good use of observational data, by the way, as the data is also a good source of data because it comes from the STS-ACC-TVT registry. and crucially, unlike some registries which are voluntary and therefore biased to the gills, this registry is mandated by law in the U.S. It therefore includes all and consecutive patients. And man, there were a lot of TAVI's done over the four-year period ending in 2023. I find this shocking, but there were nearly 360,000 TAVI procedures done in 827 hospitals in the U.S. I would have not guessed that many. There were 51,000 M-tier procedures in 493 hospitals. Now, the three main outcomes that this study was looking at was a 30-day all-cause death, a 30-day composite outcome of many, many things, death, stroke, bleeding, kidney injury, paravalvular leak, etc., etc., and then a 30-day in-hospital procedural complications. Let me first tell you some demographics. For both procedures, the median age was 79 years and nearly half were female. And before I tell you about the main differences, we should speak about the differences baseline. So for TAVR, low-volume operators were more likely to work at low-volume rural hospitals. They were less likely to do valve-in-valve TAVR, and they were less likely to do minimal or moderate sedation during TAVR. Low volume operators also had longer procedure times more use of contrast higher post gradients and more aortic insufficiency For the M tier it was much the same Low volume operators correlated with rural low volume hospitals as well as longer procedure times and slightly worse valve parameters when compared to high volume operators. Okay, and so here are the results. Low volume operators demonstrated inferior process of care measures compared with high-volume operators, and in an adjusted analysis, they also had a higher risk of 30-day mortality. 2.4 versus 2.0 percent odds ratio was 13 percent, 1.13, and those conference intervals were above one and statistically significant. In-hospital complications, odds ratio 1.09, again statistically significant. And low volume operators were considered less than 15 per year compared with high volume operators greater than 37 per year. For M tier, it was much the same story. In-hospital complications, low versus high volume, odds ratio 1.31. And here it was less than eight per year procedures compared with high volume greater than 16. While 30-day mortality was not different, Statistically, at least, the odds ratio was still 1.16, but the conference intervals went from 0.96 to 1.41. These associations were all consistent across hospital volume strata. The authors did some nice analyses where they excluded an operator's first 10 cases. This did not change the inverse associations. So, my comments. The first thing to say is that the structural heart community deserves kudos for having this kind of data. We don't have it in EP, and it would be nice, and we should have it in EP. Wouldn't you want to know low versus high volume performance for conduction system pacing, AF ablation, and VT ablation? The mandatory STS registry is one of the best healthcare policies I have seen. As you know, I am not enthusiastic about many healthcare policies, but this is a good one. Now, the first thing is, do we believe the results? Is it just noise, or is it a real association? Or perhaps is it even causal? And I think we do believe it, and I think there's probably a causal inference we can make. Why? Why do I say that? Well, you enter with a Bayesian prior that procedures are like anything in life that requires skill, and that is that practice and experience are key. Hockey players, ice skating, basketball, whatever your sport, the more you do it and the higher your volume, the better you're going to be. I also think we gain confidence in the results given the fact that they captured short-term outcomes and the data is fairly complete. But still, these are averages, right? Within those averages, there's surely lower volume operators who possibly perform better than senior operators. But in general, on average, it seems to make a difference. Now, the tension comes, though, in that even the best heavy doctor on the planet was once a low-volume operator. So there's no way to become a high-volume operator without ever being a low-volume operator. So I guess the best case is we need a very robust mentoring system where younger docs get graduated and highly supportive mentoring. But I don't even think that's the biggest tension. The whopper of all tensions comes when you try to translate this data into the face of calls to expand these procedures to underserved population. Now, I don't have the citations, but you and I have seen them. These are papers that show that black patients or poor patients or rural patients are less likely to have a TAVI center, less access to TAVI. So, this data suggests that it is surely better to concentrate procedures into places with high-volume operators. A good contrast is to contrast the U.S. situation versus a Canadian situation. For instance, in some cities in the U.S., there may be 15 procedural centers to do TAVI and M-tier. But in a large Canadian province, there may be two. While that means some patients have a long drive to the center and a long wait list, the upside is that when they have the procedure, it'll be done by a highly experienced, high-volume operator in a large center, a large center capable of dealing with complications. In my opinion, this is a better system. I would also cite here the situation with AF ablation. A person who has AFib in my city of Louisville, which is about a million people, has about eight to ten choices of where to go for their procedure. But the operator volume varies greatly. Often the place closest to the person's home, the one with the best parking lot, has the least experienced operator. So I think it's really good that the leaders in structural cardiology publish this data. Our profession should not look away from this data, and we here in the U.S. ought to consider the best way to allocate care to people. I suspect it is not lowering standards so rural hospitals can do procedures with low volume just because it's more convenient. Convenience is nice when you fly or if you stay in a hotel, but quality is far more important when people are squishing or clipping your heart valves. All right, next topic is ventricular arrhythmias in older male endurance athletes. the team in Leeds UK who did the Ventu study of older male endurance athletes have a paper in the European Journal of Preventative Cardiology on ventricular arrhythmia in older slow twitchers who insist on trashing their bodies well into old age I know this disease well there is no cure for this because it's mostly a brain disease anyways VT or non-sustained VT are important things to characterizing this group of people because VT can be both benign and malignant. The study group were 106 volunteers who were recruited via email, and I'll speak more on the matter of how they were recruited later. These men could not have had any known cardiac or medical diseases, nor could they have had any symptoms of heart disease to get into this study. They had to report exercising 10 hours per week and have done so for 15 years. Now 10 hours of exercise is a lot. I mean that means if you do a one hour ride during the work week, that's five hours, then you need to do a three and two hour rides on Saturday and Sunday. That's my normal summer load but I don't get close to that in the winter and it's a lot of riding. The volunteers had a baseline assessment with ECG, stress ECG, and CMR as well as an ILR implant. Now the ILR implant is the really cool part of the paper because of course that detects all arrhythmias. They also exercised with an exercise tracker. This was likely a Garmin watch or power meter or both and this allowed quantification of the amount of exercise. The group were legit cyclists. Their mean age was 59 years and their functional threshold power was 240 to 250 watts The findings Okay 25 of the 106 or 23 of the athletes had at least one ventricular arrhythmia Three athletes had sustained VT and 22 had non VT There were a total of 55 episodes of ventricular arrhythmia of which three were sustained VT and all three were symptomatic. There were no obvious baseline features predictive of the VT, but there were some clues from the baseline testing. For instance, on stress testing, the athletes with ventricular arrhythmia had a greater prevalence of PVCs with atypical features. FTP, a measure of one's fitness on the bike, made no difference and was not predictive of VT. However, CMR was predictive. Athletes with ventricular arrhythmia had a significantly greater prevalence of myocardial fibrosis. This was 19 versus 31 or 76 versus 38%. And all three of the people who had sustained VT had fibrosis on CMR and all exhibited PVCs with atypical features during exercise testing. Now, one of these three men got an ICD due to presyncope. One was scheduled for an EP study, and the third was advised to cease competing due to recurrent VT during exercise. Now the authors report on exercise patterns before the ventricular arrhythmia and there was not much to see there They also looked at the timing of V8 exercise and about half the time it occurred during or within an hour but none of the correlations reached statistical significance My comments This is a nice study They have most of the key elements necessary to study arrhythmia and athletes A. They had objective measures of exercise B, they had baseline data, including CMR, and they had an ILR, which is the best way to capture the outcome of interest, in this case, the ventricular arrhythmia. The first thing to say is about the exercise monitoring. One interesting side note finding, which is just of note for looking at future exercise studies, is that the athletes reported 10 hours per week, but the average amount of exercise was 7 hours per week. So when you have an objective measurement of actually how much exercise they're doing, you may find that most of these people overestimate the amount of exercise. Again, that's more of a side note finding. On the matter of the ventricular arrhythmia, I'm not a bit surprised. First, about one in five had some non-sustained VT. But you know, what I've come to observe in this modern era of monitoring with pacers and loop recorders and watches is that a few beats of non-sustained VT or atrial tachycardia is near ubiquitous. I'd love to see a project where we recruited random 60-year-olds who came out of a Walmart and put loop recorders in them. Just random people. I bet you'd see similar numbers. And I could be wrong about this, but non-sustained arrhythmias are looking more and more like a normal part of aging. I mean, we didn't know this 20 years ago because we did not have the monitoring capability like we do now. I also don't find it surprising that they had three men with structural heart disease and VT. I don't think you can say much about the incidence of this scar-related VT in the general athletic population because of the recruitment. Surely there was a bit of selection bias. To wit, let's say you're a 62-year-old. You ride a lot. you're losing watts every year because this is normal we all lose watts every year and you're like i wonder about my heart is this just aging or is this my heart or maybe perhaps you've had some funny sensations some palpitations they're not enough to see a doctor but this study being part of the study sounds like a good way to sort this out i kind of like the idea of looking at all this so i strongly suspect that these sorts of volunteer studies get enriched with people who have some inkling of something to worry about in their heart. Nonetheless, the strong correlation of ventricular arrhythmia with fibrosis is absolutely classic. Fibrosis in the heart is often arrhythmogenic for basic reasons. Recall from your old training, most VT is reentrant, and reentrant requires three things, two pathways, slowed conduction in one, and unidirectional block. This setting occurs when scar invades the myocardium. Now, the question not answerable by this study is whether the years of exercise caused the fibrosis or something else caused the fibrosis. I mean, in fact, fibrosis in the heart was one of the main reasons I was so concerned about the COVID-19 induced vaccine myocarditis. While most cases of the myocarditis after the vaccine were mild, myocarditis can lead to long-term scar, and hence you can have a predisposition to ventricular arrhythmia. But of course, anything that causes scar can lead to future ventricular arrhythmias. This is a nice study, but I would not use this data to say we need to screen older athletes. Consider, A, this was a small enriched population. B, all patients with the most serious arrhythmia had symptoms which would have led to detection of this arrhythmia and treatment before any fatal outcome occurred. Next topic is predicting cardiac risk, statin use, and what is the ideal window to look? Is it 10 years or 30 years? Last week, I got hammered on X. It was a pile-on. Why? Why? Because I dared suggest that two middle-aged woman friends who asked me to help them decide on statin use did not need to take the statins because their 10-year calculated risk was low. Here was the situation, and I look forward to comments from you all on this. Both of these friends were middle-aged, reasonably healthy women between ages high 40s and very low 60s. Both had moderately high LDLs, not near the 190 number, just moderately high, and both were told by their primary care clinician to take statins because the LDL was high. But none of them had had a risk calculation, which drives me bananas because here in Louisville, I have yet to meet a patient who've asked me about their statin use and LDL who have had such a discussion with their primary care clinician. Now, my two friends who came to me know that I have this magic calculator. I'm known for having this magic calculator that can tell them whether they need to take the statins or not. Of course, it's not a magic calculator. It's just a pooled cohort equation. Both of these ladies ended up with a 10-year risk of about 2.7%. Now, that's because they did have a high LDL, but there were not a lot of other risk factors. And of course, they're women and their ages were not super high. And so that 2 is well below that threshold level of 7 statin quote eligibility Now I put that out on X and you think I started a war Soon I was getting hammered by doctors who said this was crazy because you have to look at 30-year lifetime risk. Some of them said, come on, John, you of all people should know that atherosclerosis is a lifetime disease, and it starts early in life, and Mendelian randomization studies show that longer term exposure to lower LDL is protective and you got to start early. The basic gist of the criticism was that a decade is too short and we should treat people to protect them over 30 years from now. I thought that was, well, wait, I'll tell you later what I thought. Let's first review a study that looks exactly at this question. It comes and Circulation Outcomes on January 12th, and it's published, it's an NHANES survey from 2017 to 2020, and these were adults 30 to age 59. The first author was Timothy Anderson. What they did, their group, they described both 10 and 30-year ASCVD risk and risk vector control. They then estimated the absolute risk reduction of statin use in populations at high greater than 20% 30-year risk. Now notable is that they used the new prevent calculation score, risk score. Some will make a lot of this, but the specific calculator is not the point I want to make. The population that was studied in the CERC outcomes paper was slightly more than 3,000 adults who did not have ASCVD. The mean age was 44 years, half women, and the authors say that this 3,000 adults was representative of 100 million U.S. adults. Finding number one, the mean 10-year risk was 2.0%, and the mean 30-year risk was 9.7%. 2% versus 9.7%. Now, importantly, 9% had an elevated estimated 30-year risk of 20% or greater, and 44%, nearly half, had an intermediate estimated 30-year risk of 7.5 to 19.9%, with that elevated risk highly concentrated among individuals aged 50 to 59. Of course, because age is the biggest driver of this risk equation. All right, finding two of their paper. Of the 9% of population with high estimated 30-year risk, 33% were on statins. Finding three, most adults with a high 30-year risk had multiple uncontrolled risk factors, including blood pressure, obesity, and elevated total cholesterol. And finding four would be that if they expanded primary prevention statins to adults with a high 30-year risk, would change recommendations for 2.5 million U.S. adults not currently receiving statins with an average number needed to treat over 10 years to prevent one CV event of 78. And the authors concluded, use of the prevent 30-year ASCVD risk equation would identify a population of U.S. adults with low 10-year but high 30-year risk who may warrant enhanced primary prevention strategies. Okay, my comments. I see two sides to this argument. The authors point out that using the 10-year horizon outputs a lot of people who have one or two risk factors but a youngish age, and so they have a low risk of events, around 2 to 3%, like my two friends. This study shows that if you extend the time horizon to 30 years, then risk goes up, mainly because risk calculators turn so heavily on age. So the authors say we should treat risk factors in young people, which I agree, but they all suggest that statin use in lower risk people would likely leads to large numbers of people who avoid a cardiac event. But I have a lot of problems with this logic, a lot of problems for various reasons. Number one, if you extend the logic of this argument, where do you start? Where do you stop? You treat people with a 2% risk because it will be 9% in 30 years. Why not start earlier? Why not give statins to kids? Why not put in an infant formula. My second issue is, if you're not going to use 10-year risk calculators, then let's change the guidelines. Let's stop doing it. Right now, guidelines say statin use at 7.5%. Why do the experts choose 7.5%? Well, because statin use isn't free, right? While side effects from statins are very low, 7.5 is felt to be the threshold where experts feel the glycemic effects from statins are outweighed by the CV benefits. I don't know if it's 7.5% or 6.5 or 8.5, but it's at some threshold. Now, my third issue is 30-year timelines are ridiculously hubristic. To assume that the main thing a 40-year-old has to worry about over 30 years until he or she turns 70 is a risk of a non-fatal cardiovascular event belies common sense. We have no idea what will happen in 30 years. I think 30 years is a stupid timeline. I would also add to my argument the idea that nearly all statin trials were three to five years. How do you know the same net benefits at five years in a statin trial also applies to 30 years? You don't. It's a wild extrapolation. So my approach to my friend's 2.7% 10-year risk was to A, improve their diet, B, do regular exercise to get the HDL up and maybe reassess in a few years, in five years. The 30-year time horizon just speaks to the widespread hubris of the medical profession, I think. I mean, maybe this is what society wants from doctors. Maybe society wants us to have religious-like powers to affect things in 30 years. But I, for one, think we would do a lot better to focus on helping our patients when they get sick and perhaps avoid events over the next one to five years, a timeline which seems much more reasonable. Okay, a preview for next week where I will be taping with my portable mic from London as I am speaking at the British Cardiovascular Intervention Society meeting. Get this, get this, my main assigned talk is titled, quote, the three worst interventional trials that changed practice nonetheless. less. So here I have to thank Dr. Hildik Smith for such a great topic. By the way, I have made my three choices, but you feel free to suggest any of your favorites. The preview that I want to mention is that yesterday, yesterday, I received two notifications of some very serious complications of PFA AF ablation. I'll review those and I'll let you know about these next week and they're very provocative. Until next week, this is John Mandrola from the heart.org, Medscape Cardiology. You're listening to This Week in Cardiology from the heart.org, Medscape Cardiology. This podcast is intended for healthcare professionals only. Any views expressed are the presenter's own and do not necessarily reflect the views of WebMD or Medscape.
