Dec 12 2025 This Week in Cardiology

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 the heart.org Medscape Cardiology. And this is This Week in Cardiology for December 12th, 2025. This week...

An elegant study in post-Tavi AV block. A public service announcement for my structural heart colleagues. Revascularization in females with severe coronary disease.

a CTO PCI trial, and a top 10 review. All right, I want to start with a very elegant study on heart block during and after TAVI. and how it shows distinct patterns. This group at the Beth Israel Deaconess Medical Center in Boston have published a remarkable study from their hospital regarding the mystery of AV block after TAVR.

Now, before I tell you about this classical study of EP mechanisms, what else would you expect from the institution of the late Mark Josephson? I should set out the problem of AV block after TAVI. The problem is one of anatomy, namely the conduction system sits in close proximity to the landing area of the transcatheter aortic valve implant.

Simply stated, if you squish important parts of the conduction system, you can impede AV conduction. Think of scissors and an electric cord. Now the other main issue with AV block is one of extremes. No one wants to have a perfectly good aortic valve implant with cure of the aortic stenosis to result in a late death from delayed AV block.

Now there's no mystery when AV block occurs and persists after the procedure. This patient needs pacing simply because there are not enough heartbeats. It's easy. The main issues arise because transient AV block can occur during the procedure. or PR prolongation can occur post-procedure, or bundle branch block can occur post-procedure. All of these findings indicate some degree of injury to the connuction system.

And they make us worry about not putting in pacers. But wait, putting in a pacemaker and then have it not be used is also something we want to avoid because obviously it's not ideal to have hardware in the bloodstream. in the setting of a prosthetic aortic valve that could get infected. Now, surgical aortic valve replacement does not present the same consternation because the answer with surgical patients is much more obvious. You wait and wait.

No one cares. The patient is in pain and it is fine to stay in the hospital. There is far less pressure to discharge surgical patient at some set time. If AV connection recovers, you can often hold off on pacing. Sadly, with TAVI, cost constraints incentivize early discharge. It's crazy to me how strong this push is.

When there is a concern about delayed AV block, I'm like, just keep the patient in the hospital. I mean, in the grand scheme of health care costs, this is nothing compared to all the unnecessary stents, stress tests, PCI that happen every day. But the answer is not welcomed. So we're forced to make decisions in TAVI patients. More often than not, in gray areas, we implant a pacemaker rather than not implant because we don't want our patients to have delayed AV block and die.

Now, this dilemma is what makes the idea of simultaneous electrophysiologic evaluation during TAVI such a brilliant idea. And in a sea of inconsequential studies done to pad CVs or advance young people in academics, this paper from Beth Israel stands out as a true scientific exercise. Over a three-year period, just over 400 consecutive patients at their institution underwent TAVI, and they were studied with an EP study at the beginning and the end of the TAVR procedure.

This was accomplished simply with ECG leads and a multipolar catheter that could be used for atrial and ventricular pacing, as well as recording the all-important hispondonal electrogram. And the cool thing is that rapid pacing is required during valve deployment, and this catheter could be used for that function as well.

The primary outcome they were looking for is Mobitz type 2 or complete AV block, and this was mostly a descriptive study, but the observations are super interesting. It's in JAMA cardiology. Okay, here are some results, the basics first. 63 of 409 patients, or 15% of patients, developed AV block during the TAVI procedure, and most were complete heart block.

A.V. block was present at the end of the procedure in 19 patients, A.V. Wenkebach in 2, Mobitz 2 block in 3, and Complete Harbach in 14. Now, resolution rates. Transient block. 48 patients, 76% of the time, the block resolved during the procedure. The median duration of AV block was 2 minutes. The mean duration, 17 minutes. Persistent AV block present at the end of the procedure occurred in 15 patients, that's 24%. These were patients who received permanent pacemakers for intra-procedural block.

And 24 patients had pacemakers placed at the end of the procedure. 20 of these were temporary and four permanent pacemakers were just placed immediately. Of the 20 with temporary pacemakers, 11 had persistent block that required a permanent pacemaker, but the other 9 presumably recovered. Thus, a total of 15 patients, or 3.7%, received permanent pacemakers due to resistant heart block developing during the TAVI procedure.

post-procedure, now this is different, post-procedure in 25 patients or 6.3%. Now overall, the top five findings and lessons from this series were as follows. The delayed post-procedural block, the overall incidence, like I said, was 6.3%. This represents 25 of 394 patients who didn't have persistent intra-procedural block.

The timing of the delayed block, four patients, it occurred before hospital discharge, 21 patients block occurred after discharge, and the median timing was four days post-procedure. Now the nature of delayed block, persistent versus paroxysmal. So for paroxysmal intermittent block, this was in 20 of 25 patients. It was self-limited, averaging 11.5 seconds. Some had more prolonged episodic periods of 56 minutes to 11 hours, and only three of these 20 patients experienced syncope.

Persistent block was noted in 5 of 25 patients or 20%. What about pacemaker outcomes at follow-up? Despite all 25 patients receiving permanent pacemakers at one month, median ventricular pacing was 5.8%. Now there are five basic messages that I kind of summarize from this elegant paper.

The first is there's different mechanisms for immediate versus delayed heart block. The study revealed differences between intra-procedural and delayed block. required pacemakers at only 15 patients 3.7%, while 48 patients had transient block that resolved. In contrast, 80% of those with delayed block cases were paroxysmal intermittent, and all 25 of these delayed block patients received permanent pacemakers.

Now pacing dependency, or the percent of pacing, was different. For intra-procedural block patients that had persistent block, the median was 97.4% ventricular pacing at one month. Contrast that with delayed block patients, which was mostly paroxysmal AV block. These patients had a median of 5.8% ventricular pacing at one month.

For instance, prolonged PR interval and AV-Wenkebox cycle length pre-TAVR predicted delayed but not intraprocedural block. The length of the membranous septum was directly related to intraprocedural block, whereas delayed block... was inversely associated with membranous septal length. What about aortic annular calcium and LV outflow tract calcium burden? These were associated with intra-procedural block, but not delayed block.

And finally, the nature of the block differed between the two types. Block during the procedure tended to be persistent, whereas most delayed blocks were paroxysmal and relatively brief. As a result, models to predict delayed block will have to incorporate different variables than those identifying patients at risk for intra-procedural block. They found no predictive value of the baseline PR interval for intra-procedural block.

but baseline PR intervals longer than 200 milliseconds and end-of-procedure PR intervals longer than 300 milliseconds were associated with significantly increased risk for delayed block. Another finding from the study, both AV node and his bundle can be affected. Contrary to the common assumption that TAVR-related heart block is purely due to his bundle injury, This study documented AV nodal block in six cases during TAVR that all resolved, and in three patients, 7.5% with delayed block.

The specialized conduction system anatomic variability means the AV node can be vulnerable to compression during valve placement as well. What about pre-existing right bundle branch block? Well... A right bundle branch block predicts only intra-procedural block. So right bundle branch block before the procedure strongly predicted heart block during TAVI. Nearly 20% of those with right bundle developed persistent block during the procedure.

But surprisingly, right bundle branch block did not predict delayed block. This, if confirmed, has major implications for post-procedural monitoring strategies. HV interval, the Hisperkinje interval measured at procedure end, was the strongest predictor of delayed heart block. An HV interval greater than 80 milliseconds gave a 39% sensitivity and 84% specificity.

with excellent negative predictive value of 95%. So if you combine that with a PR interval greater than 300 milliseconds, that may provide useful risk stratification for those who we want to put in pacemakers. What about left bundle branch block? Well...

Despite widespread concern, new left bundle branch block was not associated with progression to high-grade heart block requiring pacemakers. And of course, this challenges current monitoring recommendations and suggests many patients may be observed unnecessarily.

The authors note that the 2021 European Society of Cardiology guidelines suggest it is reasonable to consider pacing... in patients with an HV of 70 milliseconds or longer, in patients with a new left bundle and a QRS duration longer than 150 milliseconds, or a PR interval longer than 240 milliseconds.

And the Beth Israel authors write that if they had followed the proposed criteria for implanting pacemakers proposed by these publications, they would have implanted multiple pacemakers unnecessarily. that is using the criteria of HV of 70 to 79 at procedure's end, and unnecessarily in 50 patients. So the authors concluded that... There indeed exist multiple anatomic, procedural, electrocardiographic, and electrophysiologic factors that influence the development of heart block after TAVR.

and it is clear that electrophysiologists can guide interventional cardiologists to place catheters to record his spinal electrograms with minimal prolongation of the TAVR procedure. And EP measurements at the end of the TAVR procedures may guide permanent pacemaker implantation beyond those provided by the ECG alone. ECG measurements combined with his bundle studies can provide physiologic data to predict delayed heart block.

Now, while these measurements, they write, have high negative predictive values, the positive predictive values remain relatively low. And our observations, they write, suggest that mechanisms for intra-procedural block differ from the... delayed block. Therefore, they require different prediction models. Finally, we have documented that both AV nodal block as well as infer nodal block may cause heart block following TAVR.

I just spent some time on that because I love this sort of work. You should read the paper. The JAMA cardiology paper is excellent. And I think this moves knowledge forward. We should have more of these kinds of studies. Rod Tug's team has done similar work looking at left-sided his Purkinje system. My friend Deraj Gupta and my friends in Hamburg and Lubeck have done work like this looking at PV reconnections after ablation.

You know, not everything has to have an RCT. Careful mechanistic work like this can add a lot. So congratulations to the authors. Now, the second topic today doesn't have a study.

I wanted to do a public service announcement to my structural colleagues. And this is it. Please, my friends, involve your friendly electrophysiologist. Let's all be friends. We're here to help. specifically two scenarios I want to talk about. One is, I've been getting messages from colleagues, and I've experienced this personally, that we were facing a situation where...

We're recommending AFib ablation in patients who already have a left atrial appendage closure device. My friends, this is a failure of thinking. Because if a patient presents with intermittent atrial fib, or recently persistent AFib, or symptoms from the AFib, and a reason not to be on long-term oral anticoagulation,

then the answer is not to do a left atrial appendage occlusion device. The answer is to send the patient to us for consideration of AFib ablation. Because if we are successful in eliminating the AFib, or reducing the AFib burden to a very low number, like those numbers in Artesia and the NOAA trials, we now have multiple studies that provide reassuring data on discontinuation of oral anticoagulation.

which is far more preferable than a left atrial appendage device plus long-term antiplatelet care. Plus, we don't love doing AFib ablation with a device in the appendage. Please, don't put a left atrial appendage closure device in patients who you think might have paroxysmal AFib amenable to ablation. The second scenario... when I ask you to phone a friend in EP, is when there is an urge to intervene on the tricuspid valve in the presence of a pacing lead. Please.

Double please, resist the urge to do anything without discussing the long-term risk of jailing or harming these pacing leads. We're here to help. We can work together.

All right, third topic is revascularization strategies in women with severe chronic coronary artery disease. Now, there have been many trials comparing PCI to CABG for patients who are recommended to have revascularization. And one way to sort out whether or not there are heterogeneous treatment effects based on sex would be to look at subgroups.

The problem is that most of the trials include so few females that there is a power issue. Now, a meta-analysis of four trials that I'll cite involved with left main disease included only 23% females. This meta-analysis is by Saventine et al., and they found no difference in the outcome of death based on sex in the subgroup analysis. There's also a Lee et al. meta-analysis in...

JAK interventions. This is a meta-analysis of the best syntax and pre-combat trials. And again, females represent only about a quarter of patients. The subgroup analyses there found no differences in outcomes. But again, this all could be due to type 2 error due to low power. Now, when there isn't data from trials, the next step can be to look at real-world observational data.

The European Heart Journal has published such an effort from a prominent team in Canada, although the senior author is Mario Gaudino from New York. They used clinical data registries from Ontario, Canada. The subjects were women who had first-time coronary revascularization, whether it was with PCI or CABG. The primary outcome was major adverse cardiovascular and cerebrovascular events.

which was all-cause mortality, MI, stroke, repeat revascularization, and the secondary outcomes included the individual components of those. The population included... 2,500 patients who had PCI, and 3,700 about who had CABG. Now, prior to matching, patients who underwent PCI were more likely to be frail and have heart failure, although they were less likely to have left main disease and had fewer vessels with significant disease.

Now, I hope you've noticed since these were not randomized, that is, a clinician chose the procedure based on patient characteristics. some of which are on spreadsheets that are available to be matched and some of which are not. The authors did propensity matching on 33 characteristics and they found three things. At a median follow-up of 5.1 years, MACE was higher with PCI compared with CABG, 1.81 highly significant conference intervals.

All-cause mortality was also higher in the group that had PCI. This was 34% higher, also statistically significant. Cardiovascular readmissions for MI, heart failure, stroke, was also higher. with PCI compared with CABG, 40% higher. Now, my comments. I would normally not cover such a study because surely patients referred for PCI in CABG differ substantially.

on baseline characteristics and propensity matching is an imperfect way to sort out differences and approximate randomization. And I've said this before, but it bears repeating. randomization is wonderful because it matches both known and unknown factors. Now, this paper though, this observational study, had some strengths worth noting.

One is that the authors did a falsification analysis and found that PCI and CABG had no effect on pneumonia and hip fracture. Now, I would have liked to have a few more falsification endpoints, but two is better than zero. This suggests that the groups were equally likely to get two common conditions of old age. The second strength in this paper, I think, is that the Kaplan-Meier curves for death took two years to separate.

And that they did not separate immediately is somewhat reassuring because Kaplan-Meier curves that separate early on things like death strongly implicate a selection bias where sicker patients get one treatment preferentially. We did not see that in this paper. The third strength is that PCI group gets way more repeat revascularizations, which is exactly what you'd also suspect.

Now, a fourth issue is that there are some biologic reasons why females might have worse outcomes with PCI. I'll quote some from the authors. They write, Women have a greater ratio of non-obstructive to obstructive CAD compared with men. That leads to a greater overall plaque burden in women compared with men for a given amount of obstructive disease. And, therefore, studies have suggested that the degree of plaque burden, rather than the extent of obstructive disease,

is a stronger predictor of future cardiovascular events. So non-obstructive plaques are not benign. As one study they cite demonstrated a majority of MIs occurred from non-obstructive plaques rather than obstructive plaques. We know that from our teaching in medical school.

And furthermore, an analysis from a registry demonstrated that women with non-obstructive left main disease had a nearly 80% higher risk for the composite of all-cause mortality, MI, or revascularization compared with men with non-obstructive left main disease.

Now, as PCI primarily treats obstructive coronary disease, whereas cabbage treats both obstructive and non-obstructive, it is plausible that the early operative risk of cabbage in women is compensated by a greater long-term reduction in MI and all-cause mortality in cabbage compared with PCI.

Now, obviously, you know the solution to this. The solution to this would come from an RCT of women. And it turns out there is such a trial, and I think I should mention it. It's called the RECHARGE trial, led by a group in New York. Recharge is government-funded. That's good. It will compare PCI and CABG in 600 women and in 600 black and Hispanic adults who have severe CAD.

The primary endpoint will be a hierarchical one with death and change from baseline and mean time average health quality of life at three years of follow-up. And, of course, since it's a hierarchical endpoint, they'll use a win ratio to... assess the effect size. Now, I laud the investigators for doing such a trial, but gosh, I worry about this endpoint. For instance, will there be enough power to sort out mortality signals? I mean, the Syntax trial enrolled 1,800 patients.

The second issue is the change in quality of life is a tough measure when two totally different types of treatments are studied. Now maybe at three years we can say it's a measurable thing. But of course, there's no perfect trial.

So good on the recharge team for doing such a trial. The next topic today is about CTO PCI. And there's been an RCT in CTO PCI. But don't get your hopes up. Jack has published the results of an RCT in patients with CTO of a coronary artery. I know what you're thinking. Thank goodness we need data on this highly invasive, resource-intensive, costly, risky procedure.

Sadly, we won't get much usable general information on the matter of doing PCI in chronic total occlusions. This trial studied a specific technique of opening a CTO. The procedure is called STAR, which stands for purposely placing a wire in a dissection plane and then re-entering downstream in the vessel. No kidding. Really, I read about this. They actually do this. Now, I learned that they used to try to...

used that wire to do a long stent in the beginning of the dissection plane, but that didn't work out so well. Now they do a balloon and come back later after healing to try to use a shorter stent. And this trial simply compared coming back at 5 to 7 weeks versus 12 to 14 weeks. Coming back sooner ended up being better. The primary endpoint, get this, was partial technical success of the stage procedure.

defined as TIMI flow grade 2 to 3 with less than 30% residual stenosis into at least one greater than 2.5 millimeter distal branch. There wasn't a statistically different rate of the primary endpoint of partial success. It was 83% versus 71%. Thankfully, there were a few serious complications. My comments on this paper. I'm merely an outside observer here, a neutral Martian, but I have some questions for my interventional colleagues. First question.

I may have missed a trial that showed that PCI, in addition to medical therapy, improves outcomes over medicine alone. Help me here. Is there one? I mean, there's Courage, there's Berry 2D, there's ischemia. They all seem to show medical therapy is quite good. Now, even in patients with severe multi-vessel CAD and left ventricular dysfunction with myocardial viability, literally the perfect patient for revascularization, the Revive BCIS team,

could not find a benefit for PCI over medical therapy. And these were all trials where PCI was feasible and mostly straightforward, not CTOs. Okay, my second question. I also may have missed the sham-controlled trial of CTO-PCI for the relief of angina over medical therapy, because surely you don't want me to believe that a trial of patients with angina

where one group gets a double-secret complex PCI and the other group gets some white tablets, has any validity for symptom relief? Third question. Since so many people are doing CTO PCI with all these neat techniques, Surely there must be a trial showing it is worth it in terms of better outcomes. Now, I remember reporting on a decision CTO trial.

which randomized more than 800 patients with CTO and found nearly the same rate of MACE events in the medicine versus PCI arm, and stunningly no difference in quality of life either. To me... It seems like CTO-PCI ought to first be shown effective in a proper trial before embarking on all these costly, risky procedures. I mean, the STAR technique seems really nifty, but to what end?

Plus, in this trial, nearly one in five patients did not have success despite two procedures oodles of radiation in contrast. I think CTO PCI should be studied not only for efficacy, or cost efficacy for that matter, but also for safety. As there are multiple papers, I'll cite one in the American Journal of Medicine showing that CTO procedures...

have substantially higher rates of major complications compared with non-CTO PCI. Now, I want to remind everybody, this is exactly like left atrial appendage occlusion. The patient with a CTO... who is treated with medical therapy in an exercise program, incurs zero procedural risk. It's something to remember.

And the final topic today is just a reminder that I'll have my top 10 stories piece for 2025 going up soon. In this piece, which I write every year, I go through and I find 10 of the top stories. They're not all trials. Some of them are stories. And it does end up being a long piece of like 2100 words. You don't have to read it all at once. Each section is only 100 to 200 words. So don't be triggered by the length of it.

I wonder if you'll agree and if in the comments, if you think I missed something that was a top 10 story, do let me know. So that's it for this week in cardiology. As always, I'm grateful that you listened. Thank you. And remember, if you like this podcast, take the time, give us a rating, write us a review. This helps others find us. Until next week, this is John Mandrola from the heart.org Medscape Cardiology.

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.