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Welcome to EP Edge Journal Watch, where cardiac electrophysiology meets evidence, precision, and perspective.
Hosted by Dr. Niraj Sharma, this weekly podcast distills high-impact cardiovascular and Cardiac Electrophysiology and arrhythmia research into clear, clinically meaningful insights. Each episode goes beyond headlines and abstracts to uncover what new studies actually mean for patient care, decision-making, and the future of electrophysiology.
What EP Edge Journal Watch stands for:
Evidence-based practice
Precision electrophysiology, arrhythmias analysis
A forward-thinking, edge-driven approach to how we interpret and apply data in real-world clinical settings.
Whether you’re an electrophysiologist, cardiologist, researcher, trainee, or allied health professional, EP Edge Journal Watch brings you the signal not the noise. Expect sharp summaries, thoughtful commentary, and practical takeaways designed for the busy clinician who wants to stay ahead of the curve
This program is for educational purposes only and reflects independent editorial commentary. It is not medical advice and should not replace clinical judgment or review of primary sources and guidelines. The views expressed are those of the host and contributors.
Niraj Sharma:Hello and welcome to EP Edge Journal Watch Issue 32. I'm Doctor. Niraj Sharma and I'm delighted to have you with me. Before we begin, I'd like to thank everyone who continues to send questions, comments and suggestions. Your ideas genuinely help shape EP Edge and your continued support has made everything we're building possible.
Niraj Sharma:Wherever you're listening, I hope the season is treating you well. In the Northern Hemisphere summer is in full swing, with long days and hopefully a little time to recharge. In the Southern Hemisphere it's the middle of winter so perhaps this episode can accompany a warm drink and a quiet break from the cold. There's a great deal happening at EP Edge and I'm excited to share some of it with you. First please look out for another collaborative edition of EP Edge Journal Watch with the Heart Rhythm Society.
Niraj Sharma:It'll be our third Journal Watch issue this month and we're looking forward to bringing you another carefully selected collection of clinically important electrophysiology research. We also have a major announcement approaching the release of the EP Edge app. The app will bring the wider EP Edge ecosystem together in one accessible place, including our podcasts, newsletters, EP Edge Rx, EP Edge Academy, educational tools, and several other features designed for both clinicians and patients. Alongside the app, the new epedge.org website will also be arriving soon. The mission behind EP Edge is simple but important: to make reliable, clinically meaningful knowledge easier to find, understand and use so that it can support better decisions and ultimately better care for our patients.
Niraj Sharma:None of this would have been possible without your encouragement, engagement, and continued support. So once again, you for being part of the EP Edge community. There's much more to come and I'm genuinely excited to share it with you. Now, let's turn to this month's studies. We'll begin with one of the most consequential questions following AF ablation: When the rhythm appears controlled, can anticoagulation safely be discontinued?
Niraj Sharma:Lucas Barbosa and colleagues addressed that question in a systematic review and meta analysis published in the August 2026 issue of Heart Rhythm. The study was needed because ablation can reduce AF burden, but stroke risk isn't created by rhythm alone. Age, prior stroke, vascular disease, and atrial cardiomyopathy still matter. Meanwhile, indefinite anticoagulation carries a real bleeding burden. The authors combined 32 studies involving more than two hundred and seventy one thousand patients.
Niraj Sharma:About one third stopped anticoagulation. They reconstructed time to event data and examined subgroups by CHADS VASc score and sinus rhythm. Across the full population, stopping anticoagulation wasn't associated with a statistically significant difference in thromboembolism. The odds ratio was zero point nine zero, with a 95% confidence interval from 0.68:1.20. The data were compatible with modest benefit, no difference, or modest harm.
Niraj Sharma:Mortality also didn't differ significantly. Bleeding moved much more clearly. Major bleeding was about sixty five percent lower in the group that stopped anticoagulation, with an odds ratio of zero point three five. That translated to roughly twelve fewer major bleeds per 1,000 patients in the pooled estimate. But the average result concealed the clinically important subgroup.
Niraj Sharma:In patients with a CHASVAS score above two, stopping anticoagulation was associated with more thromboembolic events. Here is the EP Edge take. This supports individualized discussion in carefully selected, rhythm controlled, lower risk patients. It doesn't support routine withdrawal in higher risk patients, especially with prior stroke or persistent atrial disease. Most evidence was observational, monitoring varied, and certainty was low.
Niraj Sharma:Successful ablation matters but it isn't a substitute for full stroke risk assessment. This paper lines up the ThiAlone AF and the OCEAN trials, suggesting a shared decision of stopping anticoagulation post AF ablation in patients with low CHADS VASc scores. If you'd like the detailed subgroup figures and limitations, they're laid out in the written EP Edge Journal Watch newsletter. Now let's move from the cost of anticoagulation to the cost of waiting for ablation. Dennis Keska and colleagues writing in the August 2026 issue of Heart Rhythm asked whether long waits for AF ablation drive healthcare spending.
Niraj Sharma:The intuitive answer is yes. While patients wait, they may return to the emergency department, undergo cardioversion, or be hospitalized, but longer observation also creates more time in which costs can accumulate. This observational study included eight thousand four hundred three first AF ablations in Ontario from 2016 through 2023. Investigators separated diagnosis to referral from referral to ablation time, then examined costs before ablation, and for one year afterward. The median time from diagnosis to ablation was twenty nine months.
Niraj Sharma:Median pre ablation cost was just over CAD15000 and median cost during the year after ablation was just under $20,000 including the procedure. Each additional month from diagnosis to ablation was associated with 2% higher pre ablation costs. Compounded over twelve months, that's roughly twenty seven percent, but some increase is built into having longer to collect costs. Post ablation costs rose only about 01% per waiting month, while heart failure and persistent AF were stronger cost signals. The EP Edge take is that this paper doesn't make an economic case for rushing every patient to ablation.
Niraj Sharma:A twenty nine month median pathway leaves ample time for symptoms and adverse events to accumulate. Earlier referrals should be pursued for clinical benefit, not because this retrospective Ontario analysis proves dramatic savings. It included non AF costs and can't establish causation. That brings us naturally to monitoring. If we are trying to decide whether AF is truly controlled, how much does a stretch of silence actually tell us?
Niraj Sharma:Linda Johnson and colleagues explored that question in Heart Rhythm in August 2026. Their paper was titled Estimation of Atrial Fibrillation Burden as a Function of Monitoring Time without Atrial Fibrillation. Most monitoring reports say AF was seen or it wasn't. But burden may matter more than one brief episode. The investigators asked whether each additional AF free day progressively rules out meaningful burden.
Niraj Sharma:They studied eleven thousand six hundred and thirty nine U. S. Patients without persistent or permanent AF who completed at least fourteen days of mobile cardiac telemetry. Burden was modeled according to how long the monitor remained free of episodes lasting thirty seconds, six minutes, or one hour. AF was detected in about ten percent.
Niraj Sharma:After three quiet days without a thirty second episode, the probability of ultimately finding an AF burden of at least zero point one percent was only three point one percent, so three negative days excluded that burden in about ninety seven percent. Over fourteen days, zero point one percent is roughly twenty minutes. So the study didn't exclude every late, isolated episode. The statistics provide calibrated reassurance, not certainty. Three negative days make meaningful short term burden unlikely.
Niraj Sharma:They don't exclude paroxysmal AF or tell us about later burden, stroke risk, or anticoagulation safety. The EP Edge take is practical. This could help triage patch results and design post ablation surveillance. But a negative monitor shouldn't overrule a compelling clinical story. The study used one platform, covered fourteen days, and modeled observed rather than future disease.
Niraj Sharma:Now what if an apparently normal ECG could tell us who deserves that extra monitoring in the first place? John Pfeifer and colleagues tested that idea in a multicenter validation study published in the August 2026 issue of Heart Rhythm. Artificial intelligence can identify subtle sinus rhythm patterns associated with future AF. A routine test might therefore direct monitoring toward higher risk patients, but models often weaken when they leave the system in which they were developed. The Tempus ECG AF model was externally tested at three sites in four thousand and seventeen adults aged 65 or older without known AF or implanted devices.
Niraj Sharma:Charts determined whether AF or flutter was diagnosed within one year. Six percent developed AF. The model labeled three ninety one patients as increased risk and nineteen percent of them were diagnosed. That's more than three times the cohort's baseline probability, so the score clearly enriched risk. But sensitivity was only thirty one percent.
Niraj Sharma:The model missed sixty nine percent of subsequent diagnoses. Specificity was ninety two percent, limiting how many were flagged, yet roughly four out of five alerts weren't followed by recorded AF within the year. The negative result added very little reassurance. Before seeing the model, ninety four percent of the cohort remained AF free. After a negative result, that figure was ninety five percent.
Niraj Sharma:So this is neither a rule out test nor an AF diagnosis. The EP Edge take is to view increased risk as an invitation to consider monitoring when finding AF would change management. A negative result shouldn't close a persuasive clinical evaluation. We need a prospective workflow trial showing that model guided monitoring improves outcomes without excessive false positive workups. The model's developer was also deeply involved in the study.
Niraj Sharma:From a hidden signal on the surface ECG, let's move into the lab, where the next paper asks whether an electrically silent lesion is truly durable. Jonathan Na and colleagues published a fascinating pulsed field ablation study in heart rhythm in August 2026. Immediately after PFA, tissue can be irreversibly injured, reversibly electroporated, or simply stunned. Bipolar voltage may disappear in each situation. The operator sees silence but tissue may recover.
Niraj Sharma:What's needed is a real time marker of durable injury. The investigators focused on the unipolar electrogram and terminal S wave loss. Using a pentaspline PFA catheter, they analyzed more than 8,600 electrograms in 10 patients, watched lesion recovery over fifteen minutes, used esophageal signals as an indirect epicardial view, and tested the threshold in twenty one redo patients. A unipolar voltage of 0.4 mV or less best identified S wave loss. The area under the curve was 0.91, indicating strong separation against that electrical reference.
Niraj Sharma:The wider low voltage halo shrank over fifteen minutes, while the smaller 0.4 mV core was more stable, particularly after rotated double applications. The most compelling result came at redo. Sites that later recovered conduction had shown higher unipolar voltage during the original procedure, about 0.69 versus 0.33 mV. Remarkably, the redo analysis selected the same 0.4 mV threshold, with 88% sensitivity and 88% specificity. The EP Edge take is that a 0.4 mV unipolar map may expose viable tissue hidden inside a reassuring bipolar map, But it isn't a universal endpoint.
Niraj Sharma:The threshold used electrical surrogates, not histology, one PFA platform, and a small selected redo cohort. A trial should now test whether unipolar guided completion reduces reconnection without unnecessary injury. And that raises a broader mapping question: When voltage mapping and MRI show a scar, are they really showing us the same thing? Michele Casella and colleagues examined that question in the July 2026 issue of JACC Clinical Electrophysiology. Non ischemic scar can be intramural, subepicardial, patchy, and inaccessible from the mapped surface.
Niraj Sharma:Late gadolinium MRI shows architecture in-depth. Bipolar voltage emphasizes local activity. Unipolar voltage sees deeper but less specifically, and omnipolar mapping reduces directional dependence. The investigators asked where these methods agree. They studied thirty six patients with non ischemic cardiomyopathy, ventricular arrhythmias, and visible MRI scar.
Niraj Sharma:High density omnipolar and bipolar maps were compared with endocardial MRI layers across nine segments, while unipolar maps were compared with epicardial layers. For endocardial scar location, omnipolar mapping achieved a kappa of 0.97 compared with 0.74 for conventional bipolar mapping. Kappa measures agreement beyond chance, so 0.97 means the methods almost always place scar in the same broad segment. It does not mean they agreed at every millimeter. Scar size was less precise.
Niraj Sharma:Even omnipolar mapping had a 39% median absolute error for the border zone. Unipolar mapping showed high agreement with epicardial MRI, but its confidence interval ranged from 0.36 to 1.00. With thirty six patients, the headline is less secure than it looks. The EP Edge take is that omnipolar mapping aligned better with MRI defined endocardial scar than bipolar mapping, while unipolar voltage offered clues to deeper substrate. Mapping can't replace MRI because the technologies measure different biology.
Niraj Sharma:Use them as complementary interrogators. The cohort was young, mostly male, selected, and the study tested concordance, not clinical outcomes. Now we turn to three connected papers about one drug and one very long shadow, Flecainide after cast. Christopher Lee and colleagues published a systematic review in the August 2026 issue of Heart Rhythm asking how Flecainide research changed after the cardiac arrhythmia suppression trial or CAST. CAST taught us that suppressing ventricular ectopy after myocardial infarction could improve the electrocardiogram while increasing arrhythmic death.
Niraj Sharma:That lesson changed practice, and perhaps which patient investigators were willing to study. These authors asked how the research landscape shifted afterward. The review included four fifty three studies and more than one point four seven million patients, separating publications through 1989 from 1990 onward. This was bibliometric. A small case series and a national database each counted as one study.
Niraj Sharma:The change was striking: before CAST, about twelve percent of Flecainide studies focused on AF afterward, nearly half did. Ventricular tachycardia studies fell from about twenty three percent to six percent, and post infarction studies fell from roughly six percent to one percent. Prospective interventional studies dropped from seventy four percent to thirty three percent. The p values established a change in publications, not drug safety. The denominator was studies, not patients.
Niraj Sharma:And reports of life threatening events weren't standardized patient level rates. The EP Edge take is that CAST redirected the questions science was willing to ask. That helps explain today's abundance of observational inference and scarcity of randomized certainty. The paper doesn't redefine a contraindication. It shows that absent trial evidence may reflect research avoidance, not proof across every structural phenotype.
Niraj Sharma:The next paper moves from that history into real world clinical data. And its apparently favorable result requires especially careful listening. Ting Chun Huang and colleagues studied class Ic therapy after PCI in patients with newly diagnosed AF. The paper appeared in Heart Rhythm in August 2026. This is a common dilemma.
Niraj Sharma:A patient undergoes coronary revascularization, has preserved ventricular function, and later develops AF. Class Ic drugs are avoided because of cast, so amiodarone becomes the default. The study asked whether contemporary use after PCI showed obvious harm. Using Taiwan's insurance data from 2013 through 2022, three seventy five Class Ic users were compared with three thousand seven hundred and fifty matched and weighted non users. Almost eighty nine percent received propafenone and only forty two received flecainide.
Niraj Sharma:Treatment began a median two seventy five days after AF diagnosis, not immediately after infarction. Major adverse cardiovascular events occurred in twenty nine point six percent of users and forty four point six percent of non users. These are event proportions, not incidence rates. After adjustment, class I Cus was associated with a thirty six percent lower subdistribution hazard for the composite and a thirty nine percent lower hazard of death. Ventricular arrhythmia wasn't increased.
Niraj Sharma:The adjusted estimate was 0.89, with a confidence interval from 0.69 to 1.15. That's reassuring only in a limited sense. The interval still allows a fifteen percent relative increase in ventricular arrhythmia. More importantly, the large apparent reductions in death and heart failure exceed what we'd expect from the drug. That signals clinician selection, survivor effects, and unmeasured differences in ventricular function, ischemia, frailty, and anatomy.
Niraj Sharma:The EP Edge take is narrow. No overwhelming proarrhythmic signal appeared among selected patients, but that doesn't prove causal safety or reopen routine prescribing after PCI. Exceptional off label use would require documented preserved ventricular function, no active ischemia, close ECG surveillance, and explicit discussion of the evidence gap. Our third Flecainide paper asks whether the category structural heart disease is itself too blunt. Davide Genovese and colleagues published a contemporary reappraisal of Flecainide in structural heart disease in the August 2026 issue of Heart Rhythm.
Niraj Sharma:Guidelines need categories, but patients arrive with gradients. Structural heart disease might mean a recent infarct with ischemia and ventricular dysfunction, or mild hypertrophy, recovered cardiomyopathy, stable revascularized disease, or a small MRI scar. The review asked whether cast has been transported too broadly. This was a narrative review without a formal search, risk of bias framework, or pooled estimate. It synthesized cast, mechanistic studies, and modern observational cohorts.
Niraj Sharma:The numerical anchor remains cast. Flecainide increased arrhythmic death by a relative risk of three point six and total mortality by two point five. The question isn't whether CAS was wrong, it's whether that causal result in post infarction ventricular ectopy applies unchanged to a carefully phenotyped patient treated for AF. Modern observational studies in selected stable coronary disease haven't consistently shown harm, but a non significant result can reflect genuine safety, inadequate power for rare events, or avoidance of high risk patients. Only randomized evidence can separate these possibilities.
Niraj Sharma:The EP Edge take is that future decisions may become phenotype based. A proper trial would require preserved function, complete revascularization, no active ischemia, quantified scar, normal conduction, QRS surveillance and long term safety follow-up. Until then, this review doesn't permit ignoring current contraindications. It provides a blueprint for the trial we need. After three papers asking whether we sometimes avoid Flecainide too broadly, final study reminds us why the alternative we often reach for, amiodarone, demands respect.
Niraj Sharma:Doei Ryan et al examined amiodarone associated thyrotoxicosis in patients who already had hypothyroidism. Their study was published in the August 2026 issue of Heart Rhythm. Hypothyroidism might seem protective, but amiodarone can cause thyrotoxicosis through iodine driven hormone production or destructive thyroiditis, and neither is abolished by a previous hypothyroid diagnosis. The investigators quantified that risk. Using Israel's CLALET database, they studied twenty three thousand eight hundred and fifty four adults with AF and hypothyroidism.
Niraj Sharma:Amiodarone was a time varying exposure, including twelve months after the last prescription. Medical record review confirmed one hundred and seven cases. During amiodarone exposure, thyrotoxicosis occurred at three point four three events per one thousand person years compared with zero point six three without exposure. After adjustment, the hazard ratio was five point one eight, with a 95% confidence interval from 3.48 to 7.69. Relatively, that's enormous.
Niraj Sharma:But the absolute excess was two point eight events per 1,000 person years, or about zero point two eight additional cases per 100 patients followed for a year. The complication was uncommon but important. Median time to thyrotoxicosis exceeded thirty one months, with some events years into treatment. The EP Edge take is immediately actionable. Baseline hypothyroidism is not a free pass.
Niraj Sharma:Check thyroid function before treatment, during therapy, and after discontinuation because amiodarone persists in tissue. Normal early tests don't remove the long term risk. This was observational, prescriptions didn't prove ingestion, surveillance may have differed, and type one wasn't fully separated from type two thyrotoxicosis. Even so, the study supports limiting cumulative amiodarone exposure when another effective strategy is appropriate. Let's close with a rapid recap of what issue 32 adds to practice.
Niraj Sharma:After AF ablation, anticoagulation withdrawal remains a carefully individualized option for selected lower risk patients. Higher stroke risk should make us pause. Longer waits accumulated expense, but the argument for timely referral remains clinical. Three quiet monitoring days make meaningful 14 AF burden unlikely but can't exclude every late episode or future recurrence. The artificial intelligence enriched future AF risk yet missed most later diagnoses.
Niraj Sharma:It may direct monitoring but can't rule AF in or out. In the lab, a 0.4 mV unipolar threshold may distinguish durable PFA core from recovering halo. Omnipolar and unipolar maps align with MRI scar location, though not its exact boundaries. The Flecainide paper showed how CAST redirected research, offered limited observational reassurance after PCI, and made the case for a phenotype based trial. None overturns present caution.
Niraj Sharma:Finally, amiodarone increased thyrotoxicosis risk even in patients with baseline hypothyroidism, with a long latency that makes continued surveillance essential. All references and graphics are available on the LinkedIn newsletter EP Edge Journal Watch as well as on Substack at epedge.substack.com. Questions, suggestions or concerns can be emailed to epedge. Cast@gmail . com. Thank you again for listening and for continuing to be part of the EP Edge community.
Niraj Sharma:I'm Doctor. Sharma, Take care and bye for now.