Feb 13, 2026 This Week in Cardiology Podcast

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In This Week’s Podcast

For the week ending February 13, 2026, John Mandrola, MD, comments on the following topics: Ticagrelor vs prasugrel, a new LAAC device, pulsed field ablation AF results, lifestyle intervention in AF, the term “provider” vs “doctor,” and coffee.

TUXEDO-2 Trial — Ticagrelor vs Prasugrel

JAMA Cardiology has published the TUXEDO-2 trial of ticagrelor vs prasugrel plus aspirin after coronary stenting in patients with both diabetes and multivessel disease.

One twist on the randomized clinical trial of 1800 patients was that it was done in India. As a Neutral Martian, I like the study question because I see much more ticagrelor use than prasugrel. But the German government-funded ISAR-REACT 5 trial was highly significant (36% higher rate of death, myocardial infarction [MI], and stroke with ticagrelor vs prasugrel). The trial was published in 2019.

I get the fact that it’s more complex logistics with prasugrel but gee whiz, as I have said many times, it shocks me that ticagrelor use is so much greater than prasugrel. But that’s not the only knock on ticagrelor. In PLATO, which was ticagrelor vs clopidogrel, the topline was that ticagrelor reduced the primary endpoint of CV death, MI, and stroke by 16%.

But the PLATO trial came under intense criticism:

1. In US patients, there were more deaths in the ticagrelor group compared to clopidogrel — the opposite of what was seen globally. This striking regional difference led to AstraZeneca's first FDA application being rejected and raised fundamental questions about the drug's efficacy.

2. Four countries (Israel, US, Georgia, and Russia) were monitored by independent contract research organizations (CROs) rather than by AstraZeneca. All four independently-monitored countries showed numerically higher rates of the primary outcome in the ticagrelor group compared to clopidogrel, a pattern that contradicted sponsor-monitored sites.

3. There were also discrepancies between death reports submitted to the FDA (938 deaths) vs those provided to trial investigators (905 deaths). Some death causes were reclassified in ways that favored ticagrelor; clopidogrel deaths switched from "non-vascular" to "vascular" while some ticagrelor vascular deaths were switched to "non-vascular" or "unknown."

4. The unprecedented all-cause mortality reduction (HR, 0.78, 107 more lives saved) was so large it prompted the editorial "Do You Believe in Magic?" This benefit exceeded what had been seen when comparing active drugs to placebo in similar trials and seemed biologically implausible.

5. FDA reviewer Thomas Marciniak identified a fundamental paradox: if ticagrelor provided superior platelet inhibition, patients undergoing early percutaneous coronary intervention (PCI) should have benefited most — but they actually fared worse in the short term compared to clopidogrel patients, contradicting the drug's supposed mechanism of action.

My point is that ticagrelor really didn’t look much better than clopidogrel and was clearly worse than prasugrel in ISAR-REACT.

Now we have Tuxedo. This was a study with all-comers for stents (60% with MI, 21% unstable angina, 20% with chronic coronary syndrome).

The Results

At 1 year, the primary endpoint of death, MI, stroke, or major bleeding occurred in 16.6% taking ticagrelor and vs 14.2% taking prasugrel . The risk difference of 2.33 percentage points worse with ticagrelor (95% CI, −2.07 to 6.74 percentage points) failed to meet the prespecified threshold for noninferiority (P = .84).

There were numerically higher (but not statistically significant) composite of death, myocardial infarction, stroke (10.43% vs 8.63%; P = .30), and major bleeding (8.41% vs 7.14%; P = .19) with ticagrelor when compared with prasugrel.

The authors concluded that:

“in patients with diabetes and multivessel disease undergoing PCI, ticagrelor was not noninferior to prasugrel for the reduction of primary outcome at 1 year of follow-up.”

My Comments

I’ve asked colleagues why they favor ticagrelor over prasugrel and what I usually get are fairly weak answers. Often about logistics.

You may not want to speculate, but as a cardiologist who does not do stents, I cannot understand why ticagrelor is so dominant over prasugrel in US markets when PLATO was flawed and ISAR-REACT showed prasugrel superiority.

What is it that makes ticagrelor so sticky despite the empirical evidence? While I can’t know for sure, but there are these potential reasons. 

1. Ticagrelor had the First-Mover Advantage (which is a weak argument because dabigatran also had the first-mover in oral anticoagulants but it has been crushed by apixaban and rivaroxaban).

2. Marketing and Messaging

• AstraZeneca heavily promoted the mortality benefit from PLATO, a compelling story even if questionable. Surely it was questionable.

• The twice-daily dosing was positioned as "more consistent coverage" rather than a disadvantage

• Prasugrel's label restrictions made it seem "harder to use" despite potentially being more effective

3. Guideline Inertia

• Once ticagrelor was embedded in guidelines as Class I recommendation, changing requires substantial counter-evidence

• ISAR-REACT 5, despite being non-industry sponsored and well-designed, was treated as "just one trial"

4. Hospital Formulary Lock-In

• Once hospitals negotiate contracts and build protocols around ticagrelor, there's institutional resistance to change

• Pharmacy and therapeutics committees are often conservative about switching established therapies

5. Cognitive Biases

• Confirmation bias: Cardiologists who adopted ticagrelor early became invested in that decision

• Availability heuristic: The PLATO mortality story is memorable and repeatedly cited

• Status quo bias: "This is what we've always used and patients do fine."

The main quibble I have with Tuxedo is the choice to do non-inferiority design. There is nothing less invasive, less costly or safer with ticagrelor that would justify a study of not much worse than prasugrel.

The principal investigator, Professor Bangalore, wrote to me that the hypothesis started after ISAR-REACT 5 where in the diabetic subgroup there seem to be similar outcomes between ticagrelor and prasugrel.

Nonetheless, major adverse cardiovascular events (MACE) were better on prasugrel. Bleeding was lower on prasugrel.

I wonder what a meta-analysis of trials would like. But to me, prasugrel looks to be the better drug when doctors feel they need more than clopidogrel. Ticagrelor’s stickiness despite the evidence is a worthy of study for students of evidence-based medicine.

VERITAS Study of Dual-Seal Left Atrial Appendage Occlusion

JACC EP has published results of the VERITAS study of left atrial appendage closure (LAAC) with a newer generation dual-seal occluder made by Abbott.

Before I tell you about the single-arm study of 400 patients, we should mention the irony of calling anything in this space by the Latin word for “truth” given that the seminal regulatory trial PREVAIL missed making non-inferiority in first coprimary endpoint (stroke, systemic embolism, and CV death) against warfarin.

Enough said. LAAC like any procedure will iterate — which is good. Proponents will argue that engineering and technology will improve closure rates and this should improve outcomes. I do not doubt the former; I highly doubt the latter.

Abbott bioengineers have come up with a next-generation Amulet device. The study was designed to assess 45-day safety and performance outcomes.

It’s a single-arm study. Though they screened 650 to include 400 patients. That’s sort of important because 1in 3 patients were excluded.

The implant success was very high. Near 100%. The procedure time was short at 25 minutes. Two-thirds of the patients were in sinus rhythm (SR). One-third were in atrial fibrillation (AF) (This is strange because if the two-thirds who were in SR were presumed to have paroxysmal AF, why weren’t they just ablated to get rid of AF and then stop the oral anticoagulation?)

The main findings were that device-related thrombus was found in 2.4%, major bleeding in 3.3%, any peridevice leak in 6%. A total of 2 pericardial effusions in 400 patients requiring drainage. And 24 of 400 patients did not have adequate transesophageal echocardiogram (TEE).

The authors and editorialists called these results promising. While they were clearly better than previous Amulet data, I am not sure they are that promising.

Device-related thrombus is an utter failure. Because it quadruples stroke risk and requires oral anticoagulation (OAC), which is the point of the procedure. So, to me, 2.4% is a lot of device-related thrombus (DRT) given that only super-expert implanters participated in the study. Surely a 2.4% DRT rate would be higher in less experienced hands.

Also — a PDL rate of 6% is less than ideal. And this was with TEE. Had CT been used it would likely be higher. While small leaks are better than large leaks, even small leaks increase risk of stroke.

And then there’s the business of 3.3% had major bleeds. That seems like a lot to me. How many of these patients would have had major bleeds if they went to lunch instead of having a major invasive procedure?

Now 24 of 400 patients did not have a TEE, so we have no results for 6% of the group. That’s a lot.

In sum, I am not impressed by these numbers.

Think probabilistically: Even if you were to assume some future stroke benefit or bleeding reduction from LAAC (though I do not, but let’s say there was a tiny benefit), these early complications put patients in a hole probabilistically. And this is the fatal flaw of preventive LAAC: if there is a 2%, 3%, 4%, or 5% early complication rate, there has to be an even greater percentage risk reduction in stroke or bleeding. And that’s not been clearly shown.

If I were at the FDA, I would not look favorably on these data.

Pulsed Field Ablation (PFA) vs Radiofrequency (RF) Ablation Over 4 years

As many of you know, I have been transformed from a pulsed field ablation (PFA) skeptic to PFA enthusiast. I now have done about 200 PFA AF ablations and for ablation in the left atrium, it’s quite amazing.

PFA is faster, easier on the patient, and largely devoid of the esophageal disaster worry.

But we should have data. And recently Nature Medicine has published 4-year results of the ADVENT RCT comparing PFA to thermal ablation. It’s an important question because until now, the 4 RCTs of PFA vs thermal ablation had only 1 year follow-up.

To briefly review:

• ADVENT (NEJM)                                PFA vs Thermal – no difference in efficacy

• SPHERE PER AF (Nature)                PFA vs RF – PFA noninferior to RF

• SINGLE SHOT CHAMPION (NEJM) PFA slightly better than cryoballoon

• BEAT PAROX-AF (EHJ)                    PFA similar to RF

In the original ADVENT trial about 600 patients were randomized. For this follow-up, 60% of patients (about 364) were re-enrolled at least 3 years after their initial ablation. Of these 183 were randomized to PFA and 181 to thermal ablation (about half RF and cryoballoon). Most consented to medical chart review and Holter monitor while a handful just consented to chart review.

The baseline char were similar in the two re-enrolled groups which is important because there could be bias in patients who consented vs did not consent to more follow-up.

The mean follow-up time was 3.6 years in both groups.

The main finding was that the estimated probabilities of four-year treatment success were 72.8% for PFA and 64.1% for thermal ablation (P = 0.12).

A time-to-failure analysis, evaluated by Kaplan-Meier curves, demonstrated an early decline with most failures occurring within the first 6 months, followed by a relative plateau. And then the landmark analysis demonstrates that only 9% of patients without recurrences in the first year post-PFA will have recurrences in 4-year follow-up (Fig. 2B). 

They also looked at antiarrhythmic drug use, and need for hospital-based AF treatment. And these were also similar between the two treatment strategies.

Repeat ablation was slightly higher for thermal than PFA (17% vs 10%).

As for stroke outcomes, there were 0 events in the thermal group and only 1 intracranial hemorrhage in the second year after PFA and one transient ischemic attack in year 3 in the PFA group. (These extremely low stroke rates are similar to the recent OCEAN and ALONE AF trials and is good news — and crucially it argues strongly against concomitant LAAC at the time of ablation).

My Comments

I have to compliment to Vivek Reddy and co-authors because getting longer-term data on PFA is important.

While re-enrollment could lead to bias in that those who consent to re-enroll may be different, it does seem to have been balanced in the two arms.

Even with these limitations, it does seem like the results with PFA hold up. To be sure, AF ablation remains a humbling procedure because, despite 20 years of iteration, we fail to achieve success in about a third of patients.

The authors spent a lot of words making the case that PFA may be slightly better than RF. AF burden reduction looked a bit better. The redo rates were a bit better.

I don’t think the differences are that great, but it doesn’t matter because PFA is faster, easier on patients, and comes with less worry that the patient will die at 3-4 weeks from atrioesophageal fistula. So PFA is here to stay. I can’t imagine going back to RF for AF ablation.

I still think there are iterations to be made in waveforms of electrical delivery as well as catheter types. While every company makes PFA catheters there are clearly better PFA systems in use currently. I won’t tell you which ones I believe are better because a) it’s just my opinion and b) I don’t want to get in any fights.

The final thing to say about PFA is that it has lowered the bar for who we take to the EP lab for ablation. This is both good and bad.

It’s good because I have done a handful of 90-year-olds who are back to playing golf because of the procedure.

But the fact that we’ve lowered our threshold is bad because AF is most often a systemic disease; rare is the cyclist with PV-driven AF who we cure with pulmonary vein isolation (PVI).

Instead, the typical US patient with AF has cardiometabolic issues such as obesity, hypertension, diabetes, and sleep apnea. Electrophysiologists are not proceduralists; we are doctors, and doing a 30-minute PFA ablation is not enough in many of these patients who have other conditions. 

My mantra of AF care is to give peace a chance. Just because we have PFA does not mean we shouldn’t take time to educate patients, adjust lifestyle factors, wait to see if AF will go away on its own. Taking people to the EP lab after one or two episodes of AF is definitely bad medicine.

What’s in a Name — The Use of the Term “Provider”

The American College of Physicians, who publish the Annals of Internal Medicine, have published a policy paper describing the trends, significance, and implications for patients, physicians, and health care of the use of the term provider.

This may be a US thing. I am not sure it comes up in other countries, but here in the US, doctors are increasingly being referred to as a “provider.”

As I am in my 30th year at the same hospital, I have seen the transition. When I started, the hospital was run by nurses and doctors. There were no advance practice registered nurses (APRNs) or physician assistants (PAs).

Doctors were called doctors. But....medicine has changed. Now, administrators run hospitals. Doctors are not the only humans doctoring. PAs and APRNs also provide medical care to patients.

So administrators lump us all together as providers. No kidding. They do. The two ACP authors, one a lawyer and one a doctor, attempt to make an erudite case that “provider” is bad for everyone involved. They favor “clinician” or “healthcare professional.”

I mention this piece this topic because a) it made the rounds on social media with many hundreds of accounts tweeting about it. And 11 news organizations wrote stories about this paper. And b) because it stirs emotions in many of my colleagues.

My Comments

I too was initially hacked off by the term provider. But over the years, I have come to realize that being mad when a mid-level manager calls you a provider is like being mad when it rains. It is pointless.

No matter what ACP authors write, what we are called does not matter to the patients who ask for our help. It does not matter to the person with heart block who needs me to put in a pacer at 6 PM. It does not matter to the patient with an MI who needs my colleague to get out of bed and open his LAD at 4 AM. It does not matter to the dying patient who we sit with and help ease the process.

Maybe it is my age, but I have come to believe that our calling to help people who are asking for our help is the same as it always was. And I love it just as much — perhaps more now than I ever did. The other stuff, like being called a provider or having to doing safety modules, is just noise.

But perhaps it is worth thinking about how the transition from doctor-as-a-professional to doctor-as-an-employee happened.

The first cause was when we — doctors — decided to become employees rather than independent practitioners. When I joined a private practice group we went to all the hospitals in the city. If one hospital cut cath lab staff or services, we shifted business to the other hospitals. In other words, hospitals competed for our business. They worked for us. We were our own bosses. It came with headaches because we had to hire people to do the business of medicine, but we had independence.

About 2010, with compensation changes in the US, the US doctors decided to work for hospitals. There was an initial pot of gold that came with it, and a honeymoon period where we had some control. Soon enough, though, doctors became akin to the worker who loads cones on the truck. An employee is an employee.

The second cause of the “provider” moniker came when we decided to embrace shift work. In days of old, a doctor saw patients in the hospital, then went to clinic, then went back to the hospital, and shared in a call schedule. A doctor was definitely not an employee then.

As we increasingly went to working shifts, which is clearly better for lifestyle, we lost the continuity of being commander of the ship for specific patients.  It’s easier to be called a provider when you leave at 5 PM and someone else takes care of your patient.  I am not saying I would want to go back to the old way, because it was hard to miss kids’ ball games and other things, but the new world of doctoring has downsides — and one minor one is being called a “provider.”

Coffee and Dementia Risk

• Coffee and Tea May Protect Against Dementia but Hold the Decaf

Nearly 10 years ago, I wrote a too-long essay calling for the end of coffee and blueberry research. I called it a distraction to doing other important work.

Here’s the thing: no one listened. Almost every month, there is some observational, nonrandomized, correlational study published on coffee or chocolate or quinoa or bike helmets or whatever.

Well. To my surprise, this week, JAMA, perhaps the second or third most important medical journal in the world, published another one of these observational studies looking at coffee and tea consumption and the risk of dementia.

And also to my surprise, the authors are Harvard scientists.

But not to my surprise was that higher caffeinated coffee use was associated with lower dementia risk.

The Altmetric score was 3483. More than 370 news outlets covered the story. It was even on national TV news. Thousands more tweeted about it.

But it’s utterly worthless. It was a waste of time. Its only use is as a teaching tool for evidence-based medicine classes.

Why? For two reasons. Because coffee drinkers surely have different baseline characteristics than non-coffee drinkers. And only a finite number of these confounding factors can be controlled for and adjusted for.

The larger flaw though is that it belies any common sense that one substance, such as coffee, could reduce dementia by 18%. If you believe that, you might believe an LAAC device would provide benefit.

The reason I mention this silliness is that it is a measure of the health of scientific enterprise. That Harvard researchers would do such a study — and that JAMA would publish it — indicates to me that medical science is severely sick. Instead of chasing discoveries, scientists and publishers chase attention. Clicks. News stories. Alt metric scores. I don’t have a solution, perhaps you do, but that these types of studies get done brings me sadness.

Lifestyle Interventions Post-AF Ablation

Speaking of taking care of the whole patient with AF around the time of AF ablation, a group of doctors in Eindhoven, Netherlands decided to study an integrated lifestyle intervention in an RCT.

It’s single-center, and small, but it’s an RCT and this is the way to know things in medicine.

The POP-AF trial randomized patients with AF who were to have an ablation to standard preablation counseling by an EP doctor or nurse-led integrated lifestyle clinic, including a home sleep apnea test, weight reduction, alcohol reduction, smoking cessation, and optimal hypertension and hypercholesterolemia treatment before undergoing PVI.

Only 145 patients were enrolled. The primary endpoint was a composite of hospitalization for repeat ablations and direct current cardioversions (DCCV).

PVI was done with PFA.

The trial was markedly positive. The primary endpoint occurred 52 times (492/1000 patient-years) in the control group and 25 times (240/1000 patient-years) in the lifestyle intervention group [incidence relative risk (RR) 0.49, 95% CI, 0.30–0.78, P = .004]. The rates of repeat ablations (RR, 0.43; 95% CI, 0.18–0.94; P = .045) and direct current cardioversions (RR, 0.52; 95% CI, 0.28–0.92; P = .031) were also lower in the lifestyle intervention group.

The other notable finding was similar to the Adelaide group, who first published on lifestyle interventions: It worked on metabolic risk factors. Patients in the lifestyle intervention group achieved substantial success in lowering BMI, blood pressure, LDL and improving physical activity. To me, these may be greater health benefits than reducing AF episodes.

My Comments

I like this study. I like the effort. The Adelaide group has led the way in this area, but most of their work has been observational — and while compelling, you always worry that people who decide to do the lifestyle intervention are different in ways that could improve their AF.

The other thing I like about this small trial is the endpoint. It’s not quite as hard an endpoint as an MI or stroke or death, but being admitted for repeat ablation or cardioversion captures a really clear outcome.

The limitations are obvious. It’s single center and small and it’s unavoidably open label. You could say there was performance bias, but of course, performance bias is sort of what’s being studied.

The authors note several other studies looking at the role of lifestyle interventions for AF. I am particularly curious about the role of GLP-1 drug as adjuncts to AF therapy. It may be that these drugs are equally effective to ablation in patients with AF and obesity.

Taken together with observational work from Adelaide, this study encourages us to not just destroy left atrial myocytes but attend to the metabolic health of patients with AF.

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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: Feb 13, 2026 This Week in Cardiology Podcast - Medscape - Feb 13, 2026.