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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:Hi everyone and welcome back to EP Edge Journal Watch. I m Doctor. Sharma. First, thank you for listening and as always, I really appreciate your questions and comments. They help shape how we approach these papers and, more importantly, how we translate the literature into actual electrophysiology practice.
Niraj Sharma:This is issue 37, our September 2026 edition, and there's a lot to unpack. But rather than simply giving you a list of studies and a series of numbers, I want to build the clinical story behind each paper. Why was the study needed? What uncertainty were the investigators trying to resolve? Did the methodology actually answer that question?
Niraj Sharma:When we see a risk ratio, an odds ratio, or an AUC, what does that really mean for us and for our patients? We're going to begin with the left atrial appendage, because several papers this month approached the same clinical problem from completely different angles, we'll look at what's actually happening inside the appendage, whether closure truly competes with contemporary anticoagulation, what to do after device implantation, and whether difficult anatomy simply requires a different device. Then we'll move into pulsed field ablation, including an important stroke signal and a fascinating mechanistic study of mitral isthmus transmurality. After that we'll discuss AF monitoring, cryptogenic stroke, smartwatches, postoperative AF, two practical PVC localization papers, and finally whether SGLT2 inhibitors might actually reduce sudden cardiac death. For the complete numerical results, confidence intervals, tables, references and graphics, you can always go to the full EP Edge Journal Watch newsletter.
Niraj Sharma:So let's get started. Let's begin with a paper that changes the way I think about the appendage biologically. In September 2026, lead author Ji Zhou and colleagues published Left atrial appendage thrombosis in patients with atrial fibrillation in JACC Here's the question that makes this study interesting. We know from Laos three that surgically occluding the appendage on top of usual anticoagulation reduced embolic events. So why should physically removing the appendage add anything if anticoagulation is already working?
Niraj Sharma:The investigators went directly to the tissue. They examined left atrial appendages removed from fifty seven patients in Laos three. Instead of relying on TEE or CT, they used histology and immunohistochemistry to look for microscopic thrombus, fibrin, von Willebrand factor, tissue factor, and inflammatory cells. And this is where the paper becomes fascinating: Only one appendage had a large visible thrombus. But under the microscope, twenty one of 57 (about 37% ) contained fibrin rich microthrombi.
Niraj Sharma:These were concentrated in the trabecular crypts. Fibrin deposition along the endocardium was even more common. So what does thirty seven percent mean? It does not mean that thirty seven percent of anticoagulated AF patients are about to have a stroke. It's a prevalence finding in a small surgical cohort around the time anticoagulation was interrupted but it tells us that the appendage may remain a locally thrombogenic structure at a microscopic level.
Niraj Sharma:My EP EDGE take is that this gives us a biologically plausible explanation for why mechanical exclusion might add something beyond systemic anticoagulation in selected patients. It's hypothesis generating, not practice changing by itself. And clinically, it reminds us that an appendage with no visible thrombus is not necessarily an appendage with no thrombotic biology. For the histology, exact staining findings and full limitations, take a look at the EP Edge Journal Watch newsletter. Now let's move from biology to outcomes.
Niraj Sharma:In September 2026, Leonardo Kainanic et al. Published a very focused meta analysis in the Journal of Cardiovascular Electrophysiology called Pooled Efficacy and Safety of Left Atrial Appendage Occlusion versus Direct Oral Anticoagulants or Antiplatelets. The reason this study matters is that the left atrial appendage occlusion conversation has changed. The historical question was whether closure could compete with warfarin, but that's no longer the most relevant comparison for many patients. Today the real clinical competitor is usually a direct oral anticoagulant.
Niraj Sharma:The investigators pooled four contemporary randomized trials: Prog17 Closure AF, Option and Champion AF, giving them almost five thousand nine hundred patients. The headline finding was not that one strategy simply won. The important finding was a trade off: non procedural bleeding was substantially lower after left atrial appendage occlusion. The relative risk was about zero point five five, meaning roughly a forty five percent relative reduction compared with medical therapy, but ischemic stroke moved numerically in the opposite direction. It was not statistically significant but the point estimate suggested more ischemic stroke after closure.
Niraj Sharma:That distinction is critical. A p value above 0.05 does not prove that ischemic stroke risk is identical. The confidence interval was still wide enough to include clinically meaningful harm. So I would not summarize this study by saying: Left atrial appendage occlusion is equivalent to direct oral anticoagulants. I'd say this instead: Left atrial appendage occlusion changes the distribution of risk.
Niraj Sharma:You accept an upfront procedure and device related risk, and in return you may substantially reduce bleeding that accumulates over years of anticoagulant exposure. That's how I'd use this clinically. For a patient with recurrent bleeding, that exchange may be very attractive. For somebody doing beautifully on a direct oral anticoagulants with no bleeding, it may be much less compelling. That's the EP edge take.
Niraj Sharma:This is a risk exchange strategy and patient selection is everything. The next paper looks similar but it asks a slightly different question. Ali Al Janabi and colleagues first published this analysis in August 2026 in the Journal of Cardiovascular Electrophysiology. The title is Left atrial appendage closure versus medical therapy in atrial fibrillation: a systematic review and meta analysis of randomized controlled trials. This time the investigators widened the lens.
Niraj Sharma:Instead of restricting the analysis to the contemporary trials, they included six randomized trials, adding PROTECT AF and PREVAIL to PROG-seventeen, OPTION, Closure AF, and CHAMPION AF. That gave them just over seven thousand patients. Why is that useful? Because it asks whether the entire randomized evidence base has matured enough to give us firm answers about stroke, bleeding, and mortality. Overall death, major bleeding, and total stroke were not significantly different, but again stroke subtype was interesting.
Niraj Sharma:Ischemic stroke trended higher after closure, while hemorrhagic stroke trended lower. Both had p values around 0.06. So neither result proved a difference, but both point in biologically plausible opposite directions. The investigators also performed trial sequential analysis. Think of that as asking whether the accumulated evidence has reached a large enough information size to support a firm conclusion.
Niraj Sharma:Their answer was no. That doesn't erase the original randomized trials. It simply tells us that some individual endpoints remain underpowered. There's another point I want to emphasize. This study overlaps substantially with the previous meta analysis.
Niraj Sharma:These are not two completely independent populations voting twice on the same question. My EP EDGE take is that the total evidence supports left atrial appendage closure as an established strategy in selected patients, but the exact balance between ischemic stroke reduction, hemorrhagic events, procedural risk, and long term bleeding is still being defined. In practice, the comparator matters. Beating warfarin is not necessarily the same question as competing with a modern direct oral anticoagulant. Now let's stay with the appendage but switch from pharmacology to anatomy.
Niraj Sharma:In the September 2026 issue of Europace, Lackey Reddy et al. Published the advanced LAA analysis looking at amulet implantation after Watchman screening failure. Here's the real world problem. You've decided a patient is a reasonable candidate for left atrial appendage occlusion but the anatomy is difficult. Maybe the appendage is shallow.
Niraj Sharma:Maybe it's wide, multi lobed, elliptical, or has a challenging chicken wing configuration. If one device doesn't fit that anatomy, does that mean the patient has failed left atrial appendage occlusion? Or have they simply failed one device geometry? The investigators studied six zero nine amulet implant attempts. Ninety seven patients had been considered unsuitable for Watchman, while the remaining patients were considered eligible for either device.
Niraj Sharma:Despite more challenging anatomy, amulet implantation succeeded in about ninety seven percent of the Watchman screen failure group, almost identical to the success rate in the easier anatomy group. Early clinically relevant closure was also very high. Now the safety comparisons need some restraint. The screen failure group was relatively small and the confidence intervals around clinical events were wide, so a non significant p value here does not prove that the groups had identical safety. The practical message is much simpler.
Niraj Sharma:Device specific ineligibility is not the same thing as left atrial appendage occlusion ineligibility. That's the EP edge take. If the anatomy is unfavorable for one design, another device architecture may still solve the problem. But this was not a randomized amulet versus Watchman trial, so it should not be interpreted as proving superiority of one platform. In practice, this paper reinforces the value of pre procedural imaging and anatomy driven device selection.
Niraj Sharma:The last appendage paper deals with a question almost every implanter encounters. In the September 2026 issue of Heart Rhythm, lead author Woolamiding Kaysayer et al. Published a meta analysis comparing direct oral anticoagulant therapy with dual antiplatelet therapy after left atrial appendage closure. And there's a real paradox here. We often perform left atrial appendage closure because long term anticoagulation is undesirable, but immediately after implanting a foreign device in the left atrium, we need some antithrombotic protection while that device endothelializes.
Niraj Sharma:So what's safer and more effective in that early healing period? The investigators pooled three randomized trials ADRIFT, ADLA and ANDES with seven zero four patients. The most striking result was device related thrombus. Direct oral anticoagulant therapy was associated with substantially lower odds of device thrombus than DAPT. The odds ratio was about zero point one six.
Niraj Sharma:Even more interestingly, major bleeding was also lower with direct oral anticoagulant therapy. That's counterintuitive if you start with the assumption that two antiplatelet drugs must somehow be gentler than an anticoagulant. The stroke numbers, however, were tiny. There were only a handful of events, so the study really cannot tell us whether the strategies provide equivalent stroke protection. And one statistical point: an odds ratio of zero point one six is not an 84 percentage point reduction.
Niraj Sharma:It's a relative measure. The absolute difference in device thrombus was much smaller, although still clinically meaningful. My EP EDGE take is this: don't automatically assume DAPT is the safer post left atrial appendage occlusion option. If a patient can tolerate a short course of anticoagulation, a direct oral anticoagulant based strategy may actually provide a favorable balance between thrombus prevention and bleeding, but the optimal agent, dose, and duration still need to be individualized. Now, let's change gears and move into pulsed field ablation.
Niraj Sharma:On 08/25/2026, Enrico Ferro and colleagues published an important paper in circulation: Risk of Stroke and TIA with Pulsed Field compared with Radiofrequency Ablation for Atrial Fibrillation. This study is significant because PFA has been adopted incredibly quickly, partly because of its safety narrative, and much of that narrative is justified. PFA is non thermal and may reduce certain forms of collateral injury. But safety is multidimensional. A technology can protect the esophagus and still have other procedural risks.
Niraj Sharma:This was a large prospective registry from a high volume center, including more than 4,200 AF ablation procedures. About half were PFA and half radiofrequency. The primary endpoint was clinically apparent stroke or TIA within thirty days and suspected events were reviewed by neurologists who were blinded to the energy source. The key result was a higher event rate after PFA. It was about zero point four seven percent with PFA versus zero point one percent with RF.
Niraj Sharma:After statistical adjustment, the absolute difference was about 0.36 percentage points. So what does that mean practically? Roughly speaking, in this dataset, that's around three to four additional stroke TIA events per thousand procedures. That's still a low absolute event rate, but stroke is a high consequence endpoint, and this was observational. Propensity weighting can balance measured differences but it cannot create randomization.
Niraj Sharma:PFA patients also had different lesion sets and were treated in a different procedural era. So my EP EDGE take is not that PFA is unsafe, it's that myocardial selectivity should never become a substitute for rigorous post market surveillance. We need platform specific prospective data and a better understanding of anticoagulation, sheath handling, air, thrombus formation, and lesion extent. This is exactly the kind of safety signal we should investigate, not sensationalize and not ignore. And the next PFA paper asks an entirely different question.
Niraj Sharma:In the September 2026 issue of Arrhythmia and Electrophysiology, Apur Patel and colleagues published Transmurality and Autonomic Effects of Pulsed Field Ablation on the Mitral Isthmus. This is a beautiful mechanistic paper because it challenges something we often take for granted. If the endocardial map looks blocked, is the mitral isthmus really blocked? The mitral isthmus is difficult because it's not purely an endocardial structure. Epicardial connections involving the coronary sinus and vein of Marshall can bridge what appears to be an excellent line.
Niraj Sharma:The investigators prospectively studied seventy one patients using three PFA platforms. The clever part was that they cannulated the vein of Marshall and recorded epicardial electrograms directly, so now they could test the lesion from the other side. PFA alone produced complete mitral isthmus block in only about forty five percent of patients, vein of Marshall ethanol then completed block in many more, bringing the cumulative rate to about eighty three percent. And perhaps the most interesting result was pseudoblock. In roughly thirty eight percent, the endocardial assessment could look convincing while epicardial conduction remained.
Niraj Sharma:The autonomic findings were equally interesting. Parasympathetic responses usually persisted after PFA, but were largely eliminated after ethanol. So the EP edge take is this: myocardial ablation and autonomic denervation are not the same thing. In practice, if you are creating a mitral line and the clinical stakes of durable block are high, conventional differential pacing may not tell you the whole story. Selective Marshall recordings can uncover residual conduction that the endocardial map misses.
Niraj Sharma:The future question is whether identifying and eliminating those residual pathways translates into better long term rhythm outcomes. Let's move now from ablation to rhythm detection after stroke. In September 2026, Baptiste Maili and colleagues published the PAVA score in EuropaCE. The title is Identifying Patients at Low Risk for Atrial Fibrillation after Cryptogenic Stroke, the PAVA score, and I want to make one thing clear immediately. This is not a score predicting low stroke risk.
Niraj Sharma:It predicts a lower probability of detecting AF or atrial tachycardia after cryptogenic stroke. Why was this needed? Because implantable loop recorders are very good at finding occult AF, but implanting every eligible patient has cost and resource implications. Most scores ask Who's high risk? These investigators flipped the question around and asked whether we can identify a group with sufficiently low expected diagnostic yield.
Niraj Sharma:They studied just over one thousand patients with loop recorders. PAVA stands for premature atrial contractions, age, significant valvular disease, and left atrial dilatation. In the internal validation cohort, the score discriminated reasonably well and a score of two or less identified about one quarter of patients as low risk. But here's where we need to be careful. The negative predictive value reached one hundred percent in the internal validation group, but that was based on only thirty nine low risk patients.
Niraj Sharma:In the development group, some low score patients did develop AF, and in the external validation cohort, the AUC fell to about 0.7. An AUC around 0.7 means useful discrimination, but certainly not perfect separation. My EP edge take is that PAVA may become a prioritization tool, particularly when monitoring resources are constrained. I would not use it today to tell a patient after cryptogenic stroke that they don't need monitoring. The next study needs to test the strategy itself: PAVA guided monitoring versus routine monitoring, with recurrent stroke, AF detection, treatment changes, and cost included.
Niraj Sharma:Now let's go from an implantable monitor to something millions of patients already wear. In the September 2026 issue of Europace, Martin Aguilar and colleagues reported Wearable smartwatches for atrial fibrillation detection and burden estimation after ablation: comparison with continuous monitoring. The accepted manuscript was initially published online earlier, but it appears in this September issue. This paper asks a question we are going to hear more and more often: Could a smartwatch replace the repetitive holters and patches we use after AF ablation? The investigators took continuous implantable monitor data from three forty six patients in the CIRCA dose trial and then simulated how three commercial smartwatch algorithms would have sampled those rhythms.
Niraj Sharma:That word simulated is very important. Nobody in this analysis was actually wearing the watch being tested. The Apple AF burden simulation detected about eighty two percent of recurrences. The other algorithms detected fewer, but most performed much better than short, intermittent Holter monitoring. Even more impressive was AF burden, wearable derived burden correlated extremely closely with the implanted monitor, with correlation coefficients above 0.97, but correlation isn't the same as agreement.
Niraj Sharma:The watches tended to underestimate burden somewhat, even though they ranked patients similarly. The episodes they missed generally had extremely low AF burden, which is reassuring, but the clinical importance of very low burden depends on what decision you're trying to make. My EP Edge take is that a smartwatch may eventually be an excellent scalable tool for longitudinal post ablation surveillance, particularly when the question is AF burden rather than whether a single thirty second recurrence ever occurred, But before replacing implanted monitoring in a high stakes setting, we need prospective real world comparisons that include adherence, false positives, motion artifact, and actual proprietary algorithms. For the detailed comparison with twenty four hour, forty eight hour, seven day, and fourteen day monitoring, see the newsletter. The next study brings us into postoperative AF and inflammation.
Niraj Sharma:In the September 2026 issue of Heart Rhythm, Mohammad Awad and colleagues published an updated meta analysis of the perioperative neutrophil to lymphocyte ratio or NLR as a predictor of postoperative atrial fibrillation. Why should we care about NLR? Because it's cheap, routinely available, and biologically appealing. Cardiac surgery produces inflammation, adrenergic activation, oxidative stress, atrial injury, and fluid shifts, all of which may contribute to postoperative AF. But a biomarker can be associated with an outcome and still be a poor clinical prediction tool.
Niraj Sharma:That's the important distinction in this paper. The authors pooled more than 20,000 patients. Patients who developed new postoperative AF had higher preoperative NLR. The standardized mean difference was about 0.5, meaning the two groups were separated by roughly half a standard deviation. Statistically, that's a meaningful association.
Niraj Sharma:But when the authors asked whether NLR could actually classify individual patients, performance was much more modest. Sensitivity was only about 52%, specificity about 71%, and the AUC around 0.71. In other words, if you used NLR alone, you'd miss nearly half the patients who eventually developed postoperative AF. And heterogeneity was very high, which tells us the studies differed substantially in populations, timing, thresholds and methods. My EP edge take is that NLR is biologically interesting and may add information to a larger risk model but it is not ready to be the stand alone trigger for amiodarone, colchicine or intensified monitoring.
Niraj Sharma:The better future model probably combines inflammation with age, atrial dimensions, surgical type, ECG variables and substrate markers. This paper is a great reminder that association and clinical prediction are not the same thing. Now two papers that bring us back to one of the most useful tools in electrophysiology: the 12 lead ECG. The first, led by Mesafumi Sugawara, appears in the September 2026 issue of Heart Rhythm and is titled Baseline QRS axis distinguishes parahesian PVC from outflow tract PVCs. The clinical problem is familiar: a PVC looks parahesian.
Niraj Sharma:If that's correct, it changes mapping strategy and immediately raises concerns about proximity to the conduction system. But what if the PVC only looks parahesian because the patient's baseline electrical axis is already shifted? The investigators studied 160 successfully ablated idiopathic PVCs, including 17 true parahesian PVCs, and compared the PVC axis with the patient's sinus rhythm axis. That's the elegant part. Instead of asking only What does this PVC look like?
Niraj Sharma:They asked How far did this PVC move away from this patient's own baseline? True parahesian PVCs tended to remain much closer to the sinus axis. Assigned axis difference of 18 degrees or less strongly supported parahesian origin with an AUC around 0.94, sensitivity around 94%, and specificity around 82%. A UC tells us how well the measurement discriminates between groups. 0.94 is excellent in this selected dataset, But the cohort contained only seventeen parahesian cases, excluded conduction disease and structural heart disease, and had no external validation.
Niraj Sharma:So my EP edge take is not to memorize one magic number and stop mapping, it's to adopt the concept. When you're localizing an outflow tract PVC, compare it with the sinus rhythm immediately beside it. The patient's baseline axis is part of the ECG phenotype. That may help us avoid anchoring on a parahesian diagnosis simply because of one familiar morphology. For more detailed information regarding PVC analysis, see the newsletter.
Niraj Sharma:The second ECG paper comes from Yoshihiisa Naruse and colleagues in the September 2026 issue of the Journal of Cardiovascular Electrophysiology. The title is the V6RV4R Index, a novel ECG parameter for identifying idiopathic ventricular arrhythmias originating from the aortic cusp. This answers a different localization question. Once you already suspect that a PVC is coming from the left ventricular outflow tract, where should you map first? The aortic cusps?
Niraj Sharma:The aortomitral continuity? The mitral annular region? A simple ECG clue that points you toward the best first mapping location could save time and unnecessary catheter movement. The investigator studied 159 successfully ablated LVOT ventricular arrhythmias and developed a simple ratio: the R wave amplitude in V six divided by the R wave amplitude in V four. A ratio above 0.55 favored an aortic cusp origin.
Niraj Sharma:The derivation AUC was around 0.87 and the overall finding held up reasonably well in the validation cohort. Now there's an important caution: the paper contains some inconsistencies between the narrative and tables regarding the exact sensitivity and specificity, so I would not oversell the precision of those percentages, but the directional signal is consistent. My EP EDGE take is that this can be a useful mapping priority tool. A high ratio tells you that starting around the cusp region may be reasonable. A low ratio does not rule the cusps out, and this rule should only be applied after you've already established that the arrhythmia is likely left sided.
Niraj Sharma:It isn't a substitute for activation mapping, intracardiac echo, coronary anatomy, or good EP judgement. This is exactly how I like ECG algorithms to be used. They should tell us where to look first, not where we're forbidden to look next. Our final paper takes us outside the EP lab but into a very EP relevant endpoint. In the September 2026 issue of Heart Rhythm, Andrea Matiucci et al.
Niraj Sharma:Published Impact of empagliflozin and dapagliflozin on sudden cardiac death: a systematic review and meta analysis of adjudicated randomized evidence. The question here is exciting. We already know that SGLT2 inhibitors improve outcomes across heart failure, diabetes, and chronic kidney disease. But is part of that benefit specifically a reduction in sudden cardiac death? And if it is, does that mean these drugs are somehow antiarrhythmic?
Niraj Sharma:The investigators pooled eight randomized trials containing close to 59,000 participants and focused on adjudicated sudden cardiac death. The pooled odds ratio was about zero point eight two. In conversational terms, that means the odds of sudden cardiac death were about eighteen percent lower in patients assigned to empagliflozin or dapagliflozin. The absolute difference was much smaller, roughly a fraction of one percentage point across the pooled trial populations, because sudden death was relatively uncommon. The interesting part was consistency.
Niraj Sharma:Statistical heterogeneity was essentially zero. But this does not prove a direct antiarrhythmic mechanism. None of these large trials was designed primarily to test ventricular arrhythmia suppression, reducing heart failure progression, myocardial stress, congestion, renal dysfunction, or ischemic vulnerability could all ultimately reduce sudden death without the drug behaving like a conventional antiarrhythmic agent. So my EP EDGE take is that this is a compelling signal but not a new sudden death prevention indication. The study I'd really like to see would combine clinical sudden death adjudication with ICD therapies, ventricular arrhythmia burden, fibrosis, and autonomic markers.
Niraj Sharma:That would begin to tell us why this signal exists. And again the full forest plot and statistical details are available in the newsletter. So let's quickly bring issue 37 together. JiJoe showed us that the left atrial appendage can contain microscopic thrombotic activity that conventional imaging would never reveal. Leonardo Kainnick's meta analysis reframed left atrial appendage occlusion as a trade off: less long term non procedural bleeding, but residual uncertainty around ischemic stroke.
Niraj Sharma:Ali Al Janabi's broader randomized analysis reinforced that the evidence is substantial, but not every individual endpoint is statistically mature. Lacqueridi showed us that difficult anatomy for one occluder doesn't necessarily mean failure of the entire left atrial appendage occlusion strategy. Kaysayer challenged the assumption that DAPT is automatically safer than a direct oral anticoagulant after device implantation. Enrico Ferro identified an important neurovascular safety signal with PFA that deserves prospective evaluation. Apoor Patel showed us that an apparently blocked mitral isthmus can still hide epicardial conduction and that PFA and vein of Marshall ethanol have different electrophysiologic effects.
Niraj Sharma:Baptiste Mail's PAVA score may help us think about prioritizing long term monitoring after cryptogenic stroke, but external validation reminds us not to overstate a prediction model. Martin Aguilar showed how smartwatch based sampling could dramatically improve post ablation surveillance compared with short intermittent monitors, while reminding us that simulation isn't the same as real world validation. Mohammad Awad showed that NLR carries an inflammatory signal for postoperative AF, but its standalone diagnostic performance is only moderate. Masafumi Sugawara reminded us to interpret a PVC in the context of the patient's baseline sinus rhythm axis. Yoshihisa Naruse gave us a simple V six to V four R wave ratio that may help decide where to begin mapping within the LVOT.
Niraj Sharma:And Andrea Matiuchi showed a provocative association between SGLT2 inhibition and lower sudden cardiac death while leaving the actual mechanism open for future investigation. All references and graphics are available in the LinkedIn newsletter, EP Edge Journal Watch, as well as on Substack at epedge. Substack . com. If you have questions, suggestions or concerns, email me at epedge. Castgmail . com.
Niraj Sharma:Thank you again for listening to EP Edge Journal Watch. I hope you found this useful, and I'll see you on the next episode. Take care, and bye for now.