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COMMENTARY
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only.
For the week ending April 3, 2026, John Mandrola, MD recaps 5 big trials from ACC 2026—Hi-PEITHO, PRO-TAVI, ORBITA-CTO, CHIPS-BCIS3 and CHAMPION AF.
At ACC, I sat up front during the first LBCT session. Hi PEITHO was the very first trial presented. I was there to hear CHAMPION-AF so I was not listening that actively. But what I heard was a jubilant presenter, and even more enthusiastic trial discussants. “A new era in pulmonary embolism (PE) care.” I made a note to look at this trial. Well here it is folks. Even if you aren’t a PE interventionalist, there are great trial appraisal lessons here.
NEJM published the multinational open label trial of ultrasound facilitated catheter directed fibrinolysis for intermediate-risk PE patients. Inclusion required an RV/LV ratio >1 and an elevated troponin and two indicators of cardiorespiratory (CR) distress: SBP <110 mm Hg, HR ≥ 100 bpm or RR > 20 bpm.
One group gets US-facilitated alteplase plus anticoagulation (AC) and the other gets AC alone. The primary outcome is a composite of PE-related death, CR decompensation or symptomatic PE recurrence.
PE-related death and PE recurrence are straightforward; CR decompensation was more complex. It included four items: cardiac arrest or indication for cardiopulmonary resuscitation, signs of shock (new-low BP accompanied by end-organ hypoperfusion), placement on ECMO, intubation or initiation of noninvasive mechanical ventilation, or a National Early Warning Score ( NEWS ) > 9 by two consecutive measures 15 minutes apart.
There I had to explain what CR decompensation entails, since most of the endpoints in this CR decompensation were NEWS > 9, now I have to tell you about NEWS, which of course I did not know about before looking at the trial.
NEWs is a many point score with each item ranging from 0-3 for bedside physiologic signs including respiratory rate, oxygen saturation, supplemental oxygen use, temperature, blood pressure, heart rate, and level of consciousness. Note here that the NEWS score was designed as a surveillance and escalation trigger, meaning its value was in prompting docs to act. It was never designed to be a blinded adjudicated outcome measure in a trial.
Keep in mind when I tell you the results that HI-PEITHO was open label, so clinicians knew their patient’s treatment assignment. NEWS also requires only 2 measures 15 minutes apart.
They screened 4300 patients and enrolled 544. Most were excluded for not meeting the inclusion criteria.
The maker of the EkoSonic endovascular system Boston Scientific sponsored the trial and had representation on the executive committee. Co-sponsors include the University of Mainz and the PERT consortium—which is a nonprofit receiving money from industry. The statistical analyses were performed by a contract research organization, with biostatistics planned by a Boston Scientific employee. So, in sum, 2 of the 3 funders were industry.
The two arms had about 270 patients.
A primary-outcome event occurred in 11 patients (4.0%) in the intervention group and 28 (10.3%) in the control group (relative risk, 0.39; 95% CI, 0.20 to 0.77; P=0.005). A win, right?
Now we need to look at the drivers of the primary.
PE related death higher in the active arm 3 vs 1
Recurrent PE were each 1
All the difference was CR decompensation 10 vs 28
So let’s look into the supplement and see about this 10 vs 28 difference.
Cardiac arrest and CPR was about the same 6 vs 4
Signs of shock better 5 vs 8
ECMO 1 vs 3
Intubation 5 vs 6
NEWS score > 9 2 vs 19
The primary endpoint was essentially driven by bedside score of items judged by a human clinician, like level of consciousness, taken twice 15 minutes apart.
Hard outcomes, such as PE-related death was higher, and there was no difference in PE recurrence.
14 of the 19 patients in the control arm who had [NEWS > 9] had only that as their endpoint.
On safety, major bleeding at 72 hours was 3.7% vs 1.5% (RR 2.5, 95% CI 0.8–7.9, p=0.17). The p-value is non-significant, but the trial was almost certainly underpowered to detect bleeding differences but there were 2.5x more bleeds in the intervention arm. It used thrombolytics, so it should not be a surprise, nor cast off as noise.
There was also slightly more all-cause death in the ITT population at 30 days: it was 6 vs 3.
At 30 days, the 6 minute walk test was 405 meters vs 393 meters, hardly an improvement.
The “positive” result is driven by a soft physiologic score (NEWS >9) in an open label trial. All hard endpoints were clearly not different and trended against the intervention.
Bleeding was higher
In addition, this was a highly selected population where 87% screened were not enrolled.
No overall mortality benefit and if anything, it numerically went the wrong way for the EKOS catheter.
Functional outcomes were also nearly identical.
12 month fu is planned.
I would also add that this trial was sponsored by industry. And, performed by PE interventionalists who likely believe in PE intervention
I acknowledge that PE trials are very hard to do, because presentation is often variable, and, by nature the selection has to be rigorous or you stand a chance to have too much noise—that is, patients who are not sick enough to benefit or too sick to benefit.
But I am struck by the lack of signal in important hard unbiased outcomes. The NEWS score may be good for prediction but does not seem like an unbiased trial endpoint.
I would not call this a win for ultra-sound directed fibrinolysis. Not at all. And my friends who are learning trial appraisal, this is a great example of looking deeper than topline results and studying the supplement.
The hype surrounding this trial approaches that of CHAMPION-AF.
The matter of stable CAD interests me greatly. That revascularization of these gnarly-looking lesions does not improve outcomes is one of the great mysteries of modern medicine. Trial after trial of PCI or even CABG are null. Even during an MI, the preponderance of the evidence favors culprit-only PCI and leaving the other lesions to be treated with medicine.
Yet patients with severe aortic stenosis (AS) may be different. They have left ventricular hypertrophy (LVH) and likely reduced coronary flow reserve with increased oxygen demand and a relatively reduced subendocardial perfusion. All that is without a stenosis, throw a stenosis in there and all is worse.
So the matter of revascularization of coronary flow-limiting stenosis before TAVR is a scientifically curious and clinically relevant question.
The only way to study this would be in an RCT because observational trials would be marred with tons of selection bias.
At ACC, we heard results of the PRO-TAVI noninferiority trial of deferring PCI or doing PCI before TAVI in patients with severe AS. The trial was done in the 12 centers in the Netherlands and was publicly funded.
466 patients w significant CAD were randomized to either deferral of PCI or PCI. The primary endpoint was a composite of death, MI, stroke and major bleeding at one year. It was tested with non-inferiority (NI). Whenever someone says noninferiority, the two next questions that follow are a) is it appropriate to test with NI; for instance, does the new treatment offer some less invasive or less costly approach, and b) how was the NI margin decided on.
In this case, I think NI is a great way to test deferral of PCI, as it’s clearly less invasive and less costly. The expected rate of events was 15% in both groups and the NI margin was set at 11% in risk difference. No explanation was given in the paper as to where this came about. I looked multiple times. Nothing. Why 11%. This corresponds to a relative NI margin of 1.73, meaning deferral of PCI could be 73 worse on the primary endpoint and still be deemed non-inferior.
Given NI testing, there is one more major flaw of the composite endpoint; I hope many of you see the flaw in that endpoint choice. If not, stay tuned.
Before I tell you the results there are two things to say: one is my first rule of trials: think first if the trial is trying to answer an important clinical question or sell a product. This trial is publicly funded and the question of PCI before TAVI is a true modern day question. I added the modifier “modern-day” because in days past, coronary stenoses were bypassed at the time of SAVR at little incremental risk to the patient. The availability of TAVI makes PCI or deferral of PCI a critical question.
The second thing to say is that the NOTION-3 trial, published in NEJM in 2024, found that PCI of a severe coronary stenosis vs conservative management before TAVI in patients with both AS and CAD showed a 29% reduction in the MACE endpoint of death, MI or urgent revascularization. Though the HR of 0.71 had 95% CI ranging from 0.51-0.99 and a p value of 0.04. If this was a true reduction it came at the cost of a statistically significant 51% increase in the rate of major bleeding. I tell you this because it is an important prior.
A primary endpoint of death, MI, stroke or major bleeding occurred in 24% of the deferral group vs 26% of the PCI group. The absolute risk difference using the Kaplan Meier (KM) estimates was 1.7% and the all-important 95% CI went from -9.5 to an upper bound of 6.2%, which is less than their NI margin of 11%, and, so, the deferral arm was declared NI to the PCI arm.
Another important finding was that major bleeding was substantially better at 6% vs 15%, HR 0.39.
The conclusion – in the Lancet reads as follows:
“Deferral of PCI was non-inferior to PCI before TAVI for the 1-year composite of all-cause mortality, myocardial infarction, stroke, and major bleeding. These findings suggest that an initial conservative strategy can be appropriate in selected patients, although patient-tailored treatment decisions remain essential.”
Which is opposite to the NOTION 3 results which found MACE efficacy for doing PCI.
I hate to be negative—again—but this is a faulty analysis of the data. I feel like a broken record, but, in a NI comparison, you should never put endpoints in a composite that are expected to go in opposite directions b/c they cancel each other out and NI is easier to reach. Here you have efficacy endpoints of PCI: death, MI and stroke. And you have safety endpoints: bleeding.
Let’s look at how they trend and what would have happened to NI.
The ischemic composite (death + MI + stroke) was numerically higher in the deferral group: 21% vs 16%. That’s rate difference of 4.3% with 95% CI of…wait for it…-2.7-11.4%. The upper bound of 11.4% is > than the NI margin of 11% and thus would have missed NI. The number needed to harm (NNH) = 22. What is more: the rate ratio of 1.28 or 28% more MACE had 95% CI of 0.84-1.93, so the worst case scenario would have been nearly twice as worse.
This is similar to NOTION which also had a 29% reduction in MACE in the PCI arm.
Now let’s look at safety in PRO-TAVI. Bleeding was 15% vs 6% in the PCI vs deferral group. That’s 2.5x more bleeding in the PCI arm.
In sum, when you consider deferral as the new therapy or less invasive therapy, you have substantially higher (up to 2x more) MACE events compared to revasc, at the cost of 2.5x more major bleeding, surely due to DAPT in older patients.
Again, I look at TAVI data as an outside observer, but in the case of a patient with CAD and AS, this data suggests doing PCI may decrease MACE but increase bleeding. I would not go with the PROTAVI conclusion that deferral is noninferior.
But here’s the thing, perhaps these patients with bad CAD and AS would be better served with surgery. Bypass does not substantially increase operative risk; and you only require single antiplatelet after surgery. The recommendation may be even stronger in younger patients as the EVOLUT 7 year data found a 3.6% higher death rate in TAVR vs SAVR arms.
I’d love to have a TAVI plus PCI vs SAVR plus CABG trial of patients with both. All we have now is small, underpowered subgroup analyses.
Two RCTs of chronic total occlusion (CTO) PCI vs meds (DECISION CTO and EuroCTO) have found no reduction in hard outcomes. CTO PCI is often offered to patients, mostly for angina and quality of life improvements. The evidence for benefit in this subjective endpoint however had been inconclusive. Inconclusive because no trial had done the proper test of angina relief—include a placebo procedure.
Led by Dr. Sarosh Khan and John Davies in Essex ORBITA CTO randomized 50 patients with single-vessel CTO to PCI vs a placebo procedure. As it has been done in all the ORBITA studies, extreme care was taken to maintain patient and doctor blinding.
Their efforts were successful as the blinding index revealed quite good blinding.
Inclusion criteria were strict. These were 2.5 mm vessels with J-CTO score ≤ 3. There also had to be inducible ischemia and viability and a multidisciplinary team (MDT) had to determine it be suitable. ORBITA also included only experienced operators.
The primary outcome was an angina symptom score taken on a specially designed cellphone app, called the ORBITA app. The daily angina symptom score included 3 components: episodes of angina, antianginal meds, and cardiac events like ACS or death. Follow up was 24 weeks.
The trial procedures were more similar to ORBITA 2 where antianginals were titrated up and then stopped at the time of the invasive procedure. The reasoning was to isolate the placebo-resistant angina relief.
The primary result was that CTO PCI improved angina symptom score OR 4.38 (1.57 to 12.69) Probability of benefit, Pr(benefit)= 99.6%
CTO PCI led to an additional 30.6 days free from angina (CrI 11.1 to 50.7) Pr(benefit)>99.9%
As for the components of the primary endpoint, angina frequency was the driver. It was substantially lower, whereas there was no sig difference in antianginal med use.
CTO PCI improved other measures of angina as well, such as CCS and SAQ domains of angina frequency, physical limitation, and disease specific QOL.
In hospital complications included 1 pt in the active arm who had pericarditis and one in the placebo arm who had a pseudoaneurysm treated with thrombin injection.
This is a superb trial. It was well conducted, answered an important question and the ORBITA teams from the UK have consistently shown the cardiology community that placebo-controlled procedural trials can be done.
As for the results, I would say the odds ratio of 4 for angina relief oversells the benefit. I did a 15 minute video with the authors, and they felt the degree of angina relief was moderate. That’s not nothing but moderate is moderate.
Others have criticized the choice to stop anginal meds at the time of the procedure because this is not likely what one would do in practice. Recall that in ORBITA 1, PCI was tested as an add-on to anginal meds and it had no effect over placebo. In ORBITA 2, and in this trial, meds were stopped in an effort to scientifically answer the question of whether there is any placebo resistant effect. There is, but it remains unknown how much this would add incrementally to medical therapy.
There is one interesting observation that may shed light on managing these patients in practice. That is that patients in the placebo arm enjoyed an immediate improvement from the placebo procedure. Why would that be? One reason could be placebo effect. But the other thing that Dr Davies mentioned is that it could be stopping the meds. It may be that higher perfusion pressure improved blood flow in collateral vessels. The authors plan more analyses to help sort out this finding.
Finally, it’s important to translate this data wisely. These were highly selected patients, highly selected CTOs and highly skilled operators. This moderate angina relief should not be assumed in more complex disease and sicker patients.
Kudos to the ORBITA CTO team. Again.
The microaxial flow pump is a device placed in the left ventricle that provides liters of cardiac output. Engineering wise its an incredible device. Taking blood from the LV and pumping it out into the aorta. It goes by the brand name Impella and today we break the rule against using brand names, because Impella is much easier to say than microaxial flow pump.
After its approval in 2008, through the lax 510k program, it’s had two main uses in cardiology. In AMI related cardiogenic shock and in support of high-risk PCI.
A literature search aided by LLMs estimates that between 50K-100,000 Impellas have been used for high-risk PCI. Which is the topic of today.
In 2024, the DanGer Shock trial randomly assigned 360 patients with MI-related cardiogenic shock (after screening 1211 over 10 years) to Impella use or standard care. There was a statistically fragile 26% reduction in death with the device (P = .04).
The CHIPS BCIS3 trial randomized 300 patients with severe left ventricular dysfunction and extensive severe CAD across 21 centers in the UK to Impella supported PCI or standard PCI. These were high risk patients with a median LVEF 27%; more than 80% required calcium modification and 75% had left main disease and a quarter had a CTO.
The primary endpoint was a hierarchical composite of death, disabling stroke, MI, cardiovascular (CV) hospitalization, or periprocedural myocardial injury that was analyzed with a win ratio.
Over a median follow-up of 22 months, there were 36.6% wins in the Impella arm vs 43.0% in standard care. The win ratio was 0.85 (95% CI, 0.63-1.15; P = .30).
This null result hides the main finding: Death from any cause was 54% higher in the Impella arm (32.6% vs 23.4%; HR, 1.54; 95% CI, 0.99-2.41). CV death was 91% higher with Impella (26.7% vs 14.5%; HR, 1.9; 95% CI, 1.11-3.30).
As for safety, major bleeding occurred in 10.8% of patients in the microaxial flow pump arm vs 7.3% in the standard arm (RR, 1.48; 95% CI, 0.71-3.09).
I wrote a column on this trial. Note also my rule about first asking whether the purpose of a trial was to answer a question or sell product. Here you have another example of a nonindustry funded trial designed to answer a question.
While there was clearly no benefit in a comprehensive win-ratio endpoint, there was a 12% higher rate of CV death in the Impella arm. That’s a number needed to kill of 8.
Recall that the number needed to kill in the CAST trial was 21. Which means the Impella was 3x more deadly than anti-arrhythmic drugs post MI.
The specific message is obvious: don’t use Impella for high risk PCI in patients like those in CHIPS BCIS. Guidelines should obviously downgrade this to Class 3 harm.
The larger message is 10x more important and goes to back to my feelings about medical conservatism. This device has been on the market and used for this indication for 17 years. And now, after nearly 100,000 patients have been treated, we learn that it is clearly harmful.
I am not against innovation, but new, invasive devices like Impella should be adopted after evidence. The solution is obvious: you pay for new devices only if the patient is part of a trial. Then after 1-2 years, you have proof of benefit before 17 years of harming patients takes place.
Part of the blame for this Impella debacle falls on us—the doctors. Why are we so gullible to marketing? I mean….we went to school and studied science for years, and yet we accept shoddy evidence? I don’t get it.
To those who are listening to this thinking, what about Danger Shock? There was benefit in patients with AMI and CS. My response to this is yes, but, (But), it took 10 years for PI Jacob Moller to find 360 patients suitable for this trial. And even then the 26% reduction in death was extremely statistically fragile.
And David Brown pointed out another issue to me: in the as-treated analysis which excluded 9 patients in the Impella arm who did not receive the device, and 3 patients in the standard arm who did receive the device had a HR 0.77 but CI 0.57-1.03. This is notable because if the device was conferring benefit, you would expect more benefit in the analysis where you count only patients who received the device.
Therefore, the highly selective nature of DanGer shock, its fragile statistical benefit and the nonsignificant as-treated analysis calls strongly for another trial of Impella in CS.
Again, on what planet is it right to be doing these trials 17 years after the device has been on the market? My friends, demand more not less from our industry partners.
I’ve left this for last because perhaps you’ve read my column or seen my post on X that now has 102k views.
If you haven’t heard then here is the summary. CHAMPION-AF randomly assigned 3000 patients with atrial fibrillation (AF) to either the Watchman FLX percutaneous left atrial appendage closure (LAAC) device or DOACs. These were patients eligible to take long-term anticoagulation.
Importantly these were lower risk patients than in the similar German trial CLOSURE AF. In CHAMPION, patients had a median CHADSVASC of 3.5 and a HASBLED score of only 1.3. Contrast that with CLOSURE AF where patients had a CHADSVASC of 5.2 and HASBLED of 3.1.
This study question was provocative because millions of people worldwide have AF and take oral anticoagulation to prevent stroke — a practice that rests on one of the strongest evidence bases in all of medicine. Yet, the two major challenges of anticoagulants are bleeding and adherence.
Everything wrong with this trial had to do with the endpoints and the analysis of the endpoints.
It was non-inferiority comparison for efficacy. That’s debatable because Watchman is more invasive but perhaps if it allowed a pt to avoid AC for life, NI might be reasonable.
The efficacy endpoint was stroke, systemic embolism and CV death. The first problem is that CV death is not affected by either DOAC or Watchman so it just adds noise. Yet the fatal problem with this endpoint was its analysis. Namely, the choice of NI margin of 4.8 percentage points on the absolute scale. This was based on an expected event rate of 12%; which means the authors would deem Watchman noninferior to DOACs if the upper bound of the 95% CI or worst case for stroke, SE, or CV death was no more than 4.8% higher than the DOAC arm.
But this 4.8% NI margin was based on a 12% event rate. That translates to a relative increase of 1.40 or 40% higher. Sanjay Kaul told me that most NI drug trials use a NI margin in both absolute and relative terms. CHAMPION AF authors did not; they used just absolute risk difference.
Here’s what happened: the incidence of the primary efficacy endpoint was far less than the predicted 12%, at 4.8% in the DOAC arm vs 5.7% in the Watchman arm. The absolute risk difference between the two treatments was 0.9% (95% CI, -0.8 to 2.6%). Because the upper bound of the 95% CI (worst case) was less than the margin of 4.8%, the authors declared noninferiority.
The problem is that this NI margin was based on the much higher predicted event rate. When rates come in much lower, as in this case, that 4.8% margin is far too generous. That’s why it is standard to set out both an absolute risk margin and a relative risk ratio. Like I just said, the 4.8% absolute risk increase corresponds to a 40% higher rate of the primary endpoint, so, effectively, the NI margin should also be 40%, or 1.40 in relative terms.
Table 2 of the paper shows that the 0.9% higher rate of events in the Watchman arm corresponds to a relative risk increase of 1.20. The 95% CIs were 0.87-1.66. Had the standard NI margin been used, the upper bound of 1.66 is higher than 1.40 and noninferiority would not have been met.
The components of the efficacy endpoint also looked worse for Watchman. Stroke went the wrong way. As it did in PROTECT, PREVAIL, and CLOSURE AF. In CHAMPION-AF, Stroke was 46% higher in the Watchman arm: There were 33 strokes in the DOAC group vs 50 in the Watchman arm (2.6% vs 3.3%; hazard ratio [HR], 1.46; 95% CI, 0.94-2.27). The difference in ischemic stroke was even more striking (45 vs 27; HR, 1.61; 95% CI, 1.00-2.59). The upper bound of the 95% CI of both was above 2. Hemorrhagic strokes occurred in five patients in both groups.
Some might say that the low stroke rates preclude making conclusions because of low power. Technically that is true, but I would point you to the 5% rate of device related thrombus (DRT) and the fact that 20% of patients had incomplete closure of the appendage at 4 months. Even Watchman proponent Christopher Ellis from Vanderbilt pointed this out in a post on X
Honest sobering fact here is that we need better devices before any push as front line therapy. Granted CTA picks up more vs TEE but no surprise DRT 4%+ and 20% leak rate has something to do with the ischemic stroke #. Surprising ICH was same between groups. Lower than OCEAN.
Efficacy wasn’t the only fatal flaw in this trial. Safety was also hidden by the choice of primary safety endpoint. Instead of simply counting all major bleeds in the two arms, the authors chose nonprocedural bleeding and “clinically relevant nonmajor” bleeding as the primary safety endpoint. This strongly favored the Watchman arm (10.9% vs 19%) and the authors claimed superiority for safety.
Yet, no pt can exclude procedural bleeding, which is the most common complication from this procedure. And worse, in an open-label trial, everyone knows patients on DOAC will complain of more nonmajor bleeding. The authors say these bleeds required a healthcare interaction, but unlike OPTION authors, they don’t list the actual events in the supplement.
The proper safety endpoint of all major bleeds was called a secondary endpoint and instead of testing to see if the new therapy, the Watchman was superior in safety, they tested this endpoint for noninferiority.
The results were as they always are in previous trials where all bleeds are counted: about the same. 83 patients bled in the Watchman arm vs 87 in the DOAC arm. A HR of 0.92 and clearly non-significant.
To obfuscate further, the authors created a “net clinical benefit” endpoint where they used stroke, SE, CV death and nonprocedural and nonmajor bleeding and of course this came out positive because nonmajor nonprocedural bleeding favors the device arm. A better net benefit calculation would be that there were 17 more strokes and 4 fewer bleeds in the Watchman arm. You don’t need statistics for that.
This is on the board as a win for Watchman. The company was so confident that they sent reps to our office to detail clinicians on the trial BEFORE it was released.
But while the trial sits in NEJM as a positive trial, it is clearly not. Watchman looked worse in this trial. I hold out some hope that public critical appraisal will win the day.
It would be a tragic mistake to use this trial data—especially in the face of the strongly negative LAAC data from CLOSURE AF—to offer this therapy to patients with AF on OAC.
I remind you that OAC for patients with AF is backed by some of the strongest evidence in all of Medicine. The warfarin trials showed clear benefit over placebo, and then the DOAC trials showed clear advantages over warfarin. Nearly a 100,000 patients have been randomized in trials of OAC.
I want to close by strongly pushing back against the notion pushed by proponents that we should use this data for shared decision making with patients. If this is used for SDM to convince patients to have Watchman instead of DOACs, then SDM is dead. The three overlapping circles of EBM are clinical expertise, best evidence and pt values. Well in this case, our clinical expertise and best evidence tell us to dissuade not encourage patients to choose inferior therapies over proven therapies.
And … We still don’t know whether this device has any role, because patients who struggle with OAC because of bleeding have not been studied. Based on the inferior results of CLOSURE and CHAMPION, I believe we should have a LAAC vs no OAC arm in frail older patients who cannot take OAC. That trial would likely be stopped for harm in the W arm.
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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: Apr 03, 2026 This Week in Cardiology Podcast - Medscape - Apr 03, 2026.
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Clinical Electrophysiologist, Baptist Medical Associates, Louisville, Kentucky |
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