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In This Week’s Podcast
For the week ending January 23, 2026, John Mandrola, MD, comments on the following topics: Listener feedback, the value of procedural volume for TAVR and MTEER, ventricular arrhythmia in older athletes, and the Goldilocks time horizon for predicting and modifying CV risk.
Listener Feedback
Two topics today:
Dr Jan Kleeberger from Zurich writes about my coverage of the Withdraw-AF trial, where patients with atrial fibrillation (AF)-related left ventricular (LV) dysfunction were treated and when recovered were randomized to medication withdrawal.
Kleeberger writes:
A nuance I would like to emphasize is terminology and underlying assumptions. The concept of “lone atrial fibrillation” remains controversial and is no longer supported by contemporary guidelines, largely because absence of detected disease often reflects incomplete phenotyping rather than a distinct clinical entity. Closely related, the notion of a specific “AF-mediated cardiomyopathy” is still hypothetical.
While AF burden, tachycardia, and rhythm irregularity 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.
Against that background, I worry the trial is easy to over-extrapolate. WITHDRAW-AF enrolled a small, highly selected population with recovered LVEF 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 guideline directed medical therapy (GDMT) withdrawal was short, on the order of months, which constrains our ability to assess longer-term relapse risk and myocardial remodeling trajectories.
Dr. Kleeberger’s takeaway is that:
the trial supports feasibility of carefully monitored, individualized GDMT withdrawal in select patients, with a low threshold for rapid re-initiation. 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.
I could not agree more. I pull this quote from my summary last week. I 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.
The emphasis here is, as Dr Kleeberger highlights, highly selected patients, careful withdrawal, and active surveillance.
The second comment came from Dr Douglas Rosing from NIH regarding my coverage of the amazing VECTOR procedure.
Rosing writes:
You rightly gave credit to the Emory team for achieving a successful percutaneous bypass procedure but failed to mention that the concept behind VECTOR was developed by work at the Cardiology Branch of NIH (NHLBI) and was first tested there in an animal model.
The first author on the paper you cite 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 other “first in man” procedures, including BASILICA, SESAME, LAMPOON, CATHEDRAL, transcaval aortic access, etc. I am sure you did not intentionally omit the NIH and Drs. Lederman and Bruce.
No, 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 — most often because I read manuscripts in areas where I am not an expert. Thanks for writing, Dr Rosing.
Procedural Volume and Outcomes for TAVR and MTEER
JAMA Cardiology has published a classic observational study that studies the association between an operator’s and hospital’s volume and outcomes for transcatheter aortic valve replacement (TAVR) and mitral transcatheter edge-to-edge repair (MTEER).
This is a good use of observational data — as is the source of the data, which comes the STS/ACC/TVT registry. Crucially, unlike some registries that are voluntary and therefore biased to the gills, this registry is mandated by law in the US. It therefore includes all patients.
And there were a lot of TAVRs over the 4-year period ending in 2023. I find this shocking but there were nearly 360,000 TAVR procedures done in 827 hospitals. I would not have guessed that many. There were 51,000 MTEER procedures in 493 hospitals.
The three main outcomes they measured were 30-day all-cause death, then a 30-day composite outcome of many things (30-day death, stroke, disabling bleed, VARC stage 3 acute kidney injury or paravalvular leak rated moderate to severe; MTEER: 30-day death, stroke, heart failure hospitalization, or residual mitral regurgitation of 2 or higher), then a 30-day in hospital procedural complications.
Some demographics first: For both procedures the median age was 79 years, and nearly half were female.
Before I tell you the main differences we should speak about the differences at baseline.
For TAVR:
Low-volume operators were more likely to work at low-volume rural hospitals, less likely to do valve-in-valve TAVR, and less likely to do minimal or moderate sedation during TAVR.
Low volume operators had longer procedure times, more use of contrast, higher post-procedural gradients and more aortic insufficiency.
For MTEER:
It was much the same, low volume correlated with rural, low-volume hospitals as well as longer procedural times and slightly worse valve parameters.
Low-volume operators demonstrated inferior process-of-care measures compared with high-volume operators. In adjusted analyses, a higher risk of 30-day mortality (2.4 vs 2.0%; odds ratio [OR], 1.13; 95% CI, 1.02-1.26; P = .02) and in-hospital complications (OR, 1.09; 95% CI, 1.03-1.16; P = .005) were observed for low-volume TAVR operators (less than 15 per year) compared with high-volume operators (more than 37 per year).
For MTEER, in-hospital complications (OR, 1.31; 95% CI, 1.11-1.56; P = .002) were higher for low-volume operators (less than 8 per year) compared with high-volume operators (more than 16/year). And 30-day mortality was not different (OR, 1.16; 95% CI, 0.96-1.41; P = .12). Associations were consistent across hospital volume strata.
The authors did a nice analysis where they excluded an operator’s first 10 cases. This did not change the inverse associations.
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 nice. Would you not want to know low- vs 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 — and, as you know, I am not enthusiastic about many healthcare policies, but this is a good one.
The first thing is do we believe the results? I think we do believe it. You enter with a Bayesian prior that procedures are like anything in life that requires skill — practice and experience are key. I also think we gain confidence in the results given the capture of short-term outcomes, and completeness of the data. But still, these are averages. Within those averages, there will be lower volume operators who possibly perform better than senior operators.
The tension comes, though, in that even the best TAVR doctor on the planet was once a low-volume operator. So I guess the best case is a robust mentoring system — where younger docs get graduated highly supported mentoring.
But that’s not 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 populations. I don’t have the citations but you and I have seen them: you know, the papers that show Black patients, or poor patients, or rural patients are less likely to have a TAVR center.
This data suggests that it is surely better to concentrate procedures into places with high-volume operators. You see this in our northern neighbor, Canada. In some cities in the US there are 15 procedural centers. But in a large Canadian province, there may be 2. While that means some patients have a) a long drive to the center, and b) a long wait list, the upside is that they have the procedure done by highly experienced operators in highly experienced large centers — a center capable of dealing with complications.
In my opinion this is a better system. The example I cite is AF ablation. A person in my city, Louisville, has about eight choices of where to go for their procedure. And the operator volume varies greatly. Often the place closest to a person’s home, the one with the best parking lot, has the least experienced operators.
It’s good that the leaders in cardiology published this data. Our profession should not look away, and we here in the US 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 stay in a hotel. Quality is far more important when people are squishing or clipping your heart valves.
Ventricular Arrhythmia in Older Male Endurance Athletes
The team in Leeds UK who did the VENTOUX study of older male endurance athletes have a paper in European Journal of Preventive Cardiology on ventricular arrhythmias (VA) in older slow-twitchers who insist on trashing their bodies well into old age. I know this disease well. There is no cure of this mostly brain disease.
Anyway, ventricular tachycardia (VT) or non-sustained VT (NSVT) are important things to characterize in this group of people, as VT can be both benign and malignant.
The study group was 106 volunteers recruited via email (more on the matter of recruitment later). These men could not have any known cardiac or medical disease nor could they have symptoms of heart disease. They had to exercise 10 hours per week and have done so for 15 years. Look, 10 hours is a lot. If you do a 1-hour ride during the work week, you then need a 3- and 2-hour ride on Saturday and Sunday. It’s my normal summer load but I don’t get close to that in the winter.
The volunteers had a baseline assessment with ECG, stress ECG, and cardiac magnetic resonance imaging (CMR), as well as an implantable loop recorder (ILR). The ILR implant is the cool part of this paper. They also exercised with an exercise tracker — likely a Garmin watch or power meter or both, which quantified the amount of exercise.
These were legit cyclists — mean age 59 years and average functional threshold power (FTP) of 240-250 watts.
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25 (or 23%) of the athletes had at least one VA. Three athletes had sustained VT and 22 had NSVT.
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A total of 55 episodes of VA of which 3 were sustained VT. And all 3 were symptomatic.
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There were no obvious baseline features predictive of the VT, but there were some clues from the baseline testing: For instance, on stress testing athletes with VA had a greater prevalence of premature ventricular contractions (PVCs) (21 (84%) vs 35 (47.3%) P = .001) with atypical features (14 (56%) 2 vs 11 (14.9%), P = .003).
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FTP (a measure of one’s fitness on a bike) made no difference for VT.
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On CMR, athletes with ventricular arrhythmia had a significantly greater prevalence of myocardial fibrosis (19 (76%) vs 31 (38.3%)/ and all three who had S-VT had fibrosis on CMR and all exhibited PVCs with atypical features during exercise testing. One of the three got an ICD due to presyncope and one was scheduled for an EP study, and the third was advised to cease competing due to recurrent VT during exercise.
The authors report on exercise patterns before the VA and there was not much there. They also looked at the timing of VA to exercise and about half the time it occurred during or within an hour but none of the correlations made statistical significance.
My Comments
This is a nice study. They have most of the key elements necessary to study arrhythmia in athletes — a) objective measures of exercise, b) baseline data including CMR, and that ILR is the best way to capture the outcome of interest, in this case, VA.
The first thing to say (and it is a bit of side note finding) is that the objective measures of exercise were less than self-reported — 7 vs 10 hours per week. This is important for considering other papers that use self-reported exercise time. Often an overestimate.
I am not one bit surprised about the VA. First, about 1 in 5 have some NSVT. What I have come to observe in this modern era of monitoring, with pacers, ILRs, watches, etc. is that a few beats of nonsustained VT or AT is near ubiquitous. I’d love a project where we recruited random 60 years-olds who had came out of a Walmart and put ILRs in them. I bet you’d see similar numbers.
I could be wrong about this, but nonsustained arrhythmias are probably part of normal aging. We didn’t know this 20 years ago because we did not have the monitoring capability then like we do now.
I also don’t find it surprising that they had 3 men with structural 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 surely there was a bit of selection bias. To wit: Let’s say you are 62 years old. You ride a lot. You are losing watts every year. You’re like, I wonder about my heart. Or…you know, you have had some funny sensations, not enough to see a doctor, but this study sounds a like a good way to sort this out.
So, I strongly suspect that these sorts of volunteer studies are enriched with people who have some inkling to worry about their heart.
Nonetheless, the strong correlation 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 reentry requires two pathways: slowed conduction in one and unidirectional block. This setting occurs when scar invades the myocardium.
The question not answerable by this study is whether the years of exercise caused the fibrosis or something else. Fibrosis in the heart was the reason I was so concerned about COVID-19 induced vaccine myocarditis. While most cases were mild, myocarditis can lead to long-term scar.
I like this study but I would not use this data to say we need to screen older athletes. Consider a) this was a small enriched population. And b) all patients with the most serious arrhythmia had symptoms which would have led to detection before any fatal outcome.
Predicting Cardiac Risk and Statin Use
Last week I got hammered on X / Twitter. It was a pile on. 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 them.
Here was the situation, and I look forward to any comments from you all on this. Both were middle-aged and reasonably healthy between ages high 40s and very low 60s. Both had moderately high LDL (not near 190) and both by their primary care doctor were told to take statins because of their high LDL cholesterol.
None of them had a risk calculation—which drives me bananas because here in Louisville I have yet to meet a patient who has had such a discussion. My friends knew that I have this “magic” calculator as they call it. Well, it’s not magic, it’s just the pooled cohort equation (PCE).
Both of these ladies had a 10-year risk of about 2.7%. Well below the 7.5% statin “eligibility” threshold. I put that out on X / Twitter and you’d 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 or lifetime risk. 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 longer-term exposure to lower LDL is protective.
The basic gist of it was that a decade is too short, and we should treat people to protect them for 30 years from now. I thought that was….wait, I will tell you later. Let’s first review a study that looks exactly at this question.
Circulation: Population Health and Outcomes on January 12 published an NHANES survey from 2017-2020 of adults ages 30-59. First author Timothy Anderson.
They described both 10- and 30-year atherosclerotic cardiovascular disease (ASCVD) risk and risk factor control. They then estimated the absolute risk reduction (ARR) of statin use in populations at high (>20%) 30-year risk. Notable is that they used the new PREVENT risk score. Some will make a lot of this, but the specific calculator is not the point I want to make.
The population included slightly more than 3000 adults who did not have ASCVD. Mean age 44 years. Half women. The authors say this is representative of 100 million US adults.
Finding No. 1
The mean estimated 10-year ASCVD risk was 2.0% and the mean 30-year risk was 9.7% (95% CI, 9.4%–10.1%). Importantly, 9% had an elevated estimated 30-year ASCVD risk of 20% or greater and 44% had an intermediate estimated 30-year risk of 7.5% to 19.9%, with elevated risk highly concentrated among individuals aged 50 to 59 years.
Finding No. 2
Of the 9% of the population with high estimated 30-year ASCVD risk, 33% reported statin use.
Finding No. 3
Most adults with high 30-year ASCVD risk had multiple uncontrolled risk factors, including elevated blood pressure, obesity, and elevated total cholesterol.
Finding No. 4
Expanding primary prevention statins to adults with high 30-year ASCVD risk would change recommendations for 2.5 million adults not currently receiving statins, with an average number needed to treat over 10 years to prevent one ASCVD event of 78.
Authors’ Conclusion
Use of the Predicting Risk of Cardiovascular Disease Events 30-year ASCVD risk equations would identify a population of US adults with low 10-year risk (but high 30-year risk) who may warrant enhanced primary prevention strategies.
My Comments
There are 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 to a low risk of events. Around 2%-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 also suggest that statin use in lower-risk people would likely lead to large numbers of people who avoid a cardiac event.
I have a lot of problems with this logic, for various reasons:
Number one: If you extend the argument, 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 it in infant formula?
My second issue: If you are not going to use 10-year risk calculators, then let’s change that. Stop using them. Right now, guidelines recommend statin use at 7.5%. Why? Because statin use isn’t free. While side effects from statins are very low, 7.5% is the threshold where experts feel the glycemic effects are outweighed by cardiovascular (CV) benefits.
My third issue: 30 year timelines are ridiculously hubristic. To assume that the main thing a 40-year-old has to worry about over the 30 years until he or she turns 70 is a risk of nonfatal CV event belies common sense. We have no idea what will happen in 30 years. I think 30 years is a stupid timeline, in my opinion. I would also add to my argument the idea that nearly all statin trials were 3-5 years. How do you know the same net benefits at 5 years also apply to 30 years? You don’t. It’s a wild extrapolation.
My approach to my friends’ 2.7% 10-year risk was to improve their diet, do regular exercise to get the HDL up, and maybe reassess in say 5 years.
The 30-year time horizon just speaks to the widespread hubris of the medical profession. Maybe this is what society wants from doctors. Maybe people want us to have religious-like powers to affect things in 30 years. I for one think we should do better to focus on helping our patients when they get sick and perhaps avoid events over the next 1-5 years, a timeline that is much more reasonable.
Heading to London
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. My main assigned talk is titled: The Three Worst Interventional Trials that Changed Practice Nonetheless. So here I have to thank Dr. David Hildick Smith for such a great topic. By the way, I have made my choices but feel free to suggest your favorite.
The preview is that I received two notifications just yesterday of some serious complications of pulsed field ablation. I will review and let you know next week.
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Cite this: Jan 23, 2026 This Week in Cardiology Podcast - Medscape - Jan 23, 2026.
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