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Welcome to EP Edge Journal Watch — where cardiac electrophysiology meets evidence, precision, and perspective.
Hosted by Dr. Niraj Sharma, this bi-weekly podcast distills high-impact cardiovascular and EP 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
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:Welcome back to EP Edge Journal Watch. I am Doctor. Sharma and I am glad you are here. First, I want to say thank you. I really appreciate the suggestions, comments and feedback from listeners and readers.
Niraj Sharma:That feedback helps shape how we discuss these papers, not just as abstracts, but as studies that affect what we do in the EP lab, in clinic, and in shared decision making with patients. This is Issue 28 July 2026 and this month has a very clear theme: electrophysiology is moving from new technology to evidence pressure. Pulsed Field Ablation, or PFA, is no longer just a new energy source. It is changing procedure time, lab capacity, lesion set behavior, and safety surveillance. Left atrial appendage occlusion is no longer just about whether the appendage is sealed.
Niraj Sharma:It is now about stroke protection, bleeding reduction, device related thrombus, peri device leak anatomy, and pericardial risk. And AF ablation is again confronting a familiar question: what do we do when the pulmonary veins are not the whole story? We also continue to build excitement around the EP Edge Journal Watch podcast with Heart Rhythm Society. The newsletter gives us the structure, but the podcast lets us talk through the nuance what this means in real patients, real procedures, and real decision making. So today we will move through four themes: expansive use, safety, AF beyond the pulmonary veins, left atrial appendage occlusion in the evidence era, and finally conduction system pacing.
Niraj Sharma:For the full tables, references, and graphics, the EP Edge Journal Watch newsletter has all the details. Let us start with PFA expansion. The first study asks a very practical question: What happened when PFA moved from trials into ordinary United States EP labs? This is important because pivotal trials can tell us whether a technology works under controlled conditions, but they cannot fully tell us how fast operators will adopt it, whether lab volume will change, whether safety will hold up during rapid national uptake, or whether an easier energy source will change what we choose to ablate. Freeman et al.
Niraj Sharma:Used the NCDRA Fib Ablation Registry. They looked at more than 63,000 AF ablation procedures from 158 U. S. Sites, from January 2024 through March 2025. They compared PFA, radiofrequency, cryoballoon, and combinations of these energy sources.
Niraj Sharma:The focus was utilization, procedure characteristics, adjunctive lesion sets, and in hospital safety. The result was not subtle. PFA went from essentially zero use to becoming the dominant ablation energy source. By March 2025, PFA alone accounted for about sixty one percent of AF ablations and PFA plus RF accounted for another fourteen percent. At the same time, RF alone fell sharply and cryoballoon use nearly disappeared.
Niraj Sharma:The lab also changed. Median monthly AF ablation volume rose from about twenty cases per site to twenty nine cases per site. That is not just market share, that is capacity. PFA procedures were shorter, roughly eighty nine minutes compared with about one hundred and eighteen minutes for RF. But the most provocative finding was lesion set behavior.
Niraj Sharma:Posterior wall isolation became much more common with PFA, while CTI ablation was less common with PFA alone. That tells us that technology may be shaping philosophy. The safety signal was reassuring at the in hospital level, adverse events were similar across groups, and stroke or TIA was very low, but this does not mean all energies are identical. It means that within the captured in hospital window, rapid PFA adoption did not show an acute safety penalty. The limitations are important.
Niraj Sharma:This was observational. It does not capture long term recurrence, delayed esophageal injury, vasospasm after discharge, or delayed hemolysis related renal injury. The EP Edge take is this: PFA has moved from innovation to infrastructure. That is exciting. But faster ablation changes behavior.
Niraj Sharma:The future should not be PFA lets us ablate more. The future should be: PFA lets us ablate more precisely, more safely, and only when the mechanism justifies it. The next PFA paper is the VoLTE AFIDE study, and it moves us from national adoption to device design. Here is the clinical problem: PFA is fast. But the first generation of PFA raised important practical questions: How do we assess tissue contact?
Niraj Sharma:How do we know energy is going into myocardium rather than the blood pool? Can we improve pulmonary vein isolation durability while also reducing hemolysis risk? That is where the balloon in basket design becomes interesting. This system uses an eight spline catheter integrated with an electroanatomic mapping system and tissue proximity feedback. The idea is simple but important.
Niraj Sharma:If you improve apposition at the pulmonary vein antrum, you may get better lesions, less unnecessary blood pool exposure, and more durable PVI. The study was prospective, multicenter, and non randomized. It enrolled three ninety two patients with three twenty treated in the main analysis cohort, one hundred and sixty five with paroxysmal AF, and one hundred and fifty five with persistent AF. The ablation strategy was deliberately clean, PV isolation only, no posterior wall, no extrapulmonary vein ablation, no non PV trigger ablation. There was also a required twenty minute waiting period to confirm entrance block.
Niraj Sharma:The main result was strong in paroxysmal AF and more nuanced in persistent AF. Primary effectiveness at one year was about eighty one percent in paroxysmal AF and sixty three percent in persistent AF. The safety event rate was low (about one point nine percent ), with no primary safety events in the paroxysmal AF group. What do those statistics mean? For paroxysmal AF, eighty one percent with a PV isolation only strategy is a strong signal.
Niraj Sharma:For persistent AF, sixty three percent is respectable, especially because the protocol did not allow extra substrate ablation, but it also reminds us that persistent AF is often not just a pulmonary vein disease. The redo data were also interesting. Among veins reassessed during redo procedures, most remained isolated. That suggests durability. But we have to be careful because redo patients are a selected group.
Niraj Sharma:The limitations are straightforward: single arm design, high volume operators, intermittent rhythm monitoring, no continuous AF burden assessment, and PVI only use. The EP Edge take: Volt AF brings PFA back to fundamentals: contact, geometry, durability, and safety. For paroxysmal AF, this is encouraging. For persistent AF, it may show us the ceiling of even a very good PVI only strategy. The future may be device selection by job, occlusive systems for PVI, focal tools for focal or linear lesions, and mapping to guide only the substrate that deserves treatment.
Niraj Sharma:Now let us stay with PFA but move from efficacy to safety. This third paper is a state of the art review on intravascular hemolysis and PFA. This topic matters because PFA began with a very compelling safety narrative: less thermal injury, less esophageal concern, less phrenic nerve injury, less pulmonary vein stenosis, but then real world experience surfaced a different concern: red blood cells exposed to high voltage electric fields inside blood filled chambers. The real question is not whether some hemolysis can occur. It can.
Niraj Sharma:The question is when it matters clinically and how we should measure it. Coleman et al. Reviewed human and translational PFA hemolysis studies from 2020 to 2025. Out of 53 studies reviewed, only 19 had enough biomarker or kidney injury data to assess. The authors then graded studies based on whether the right biomarker was measured at the right time.
Niraj Sharma:That timing is everything. Free plasma hemoglobin is the earliest and most direct marker. It rises within the first hour and continues rising for several hours. LDH peaks later, but it is nonspecific because ablation also injures cardiac myocytes. Haptoglobin falls as it binds free hemoglobin, usually reaching its low point later.
Niraj Sharma:Creatinine and bilirubin are downstream markers. They tell you about consequences, not necessarily the hemolytic event itself. This is why the statistics in this review are really about measurement validity. If a study only checks creatinine at twenty four hours, it might miss the actual hemolysis signal. If it checks free plasma hemoglobin early, it is much better aligned with the biology.
Niraj Sharma:The review found that laboratory hemolysis after PFA is not rare, but clinically meaningful renal injury appears uncommon. The threshold debate also matters. Some frameworks use fifty mgdL of free plasma hemoglobin, while others use one hundred. A lower threshold may detect more cases. A higher threshold may better identify more severe laboratory hemolysis, but the exact PFA specific threshold for clinical harm remains unsettled.
Niraj Sharma:This was a narrative review, not a pooled meta analysis. The included studies varied by catheter, waveform, application number, biomarker timing, hydration, renal risk, and workflow. The EP Edge take is practical. Do not panic, but do not ignore it. Hemolysis is real, usually transient and probably modifiable.
Niraj Sharma:The variables are technology, dose, contact, catheter footprint, renal reserve, hemodynamics, and hydration. Routine labs for everyone may not be necessary. Selective vigilance in higher risk patients and higher dose procedures is the smarter path. Now we shift from PFA to a much older and still unresolved AF question: What about triggers beyond the pulmonary veins? Pulmonary vein isolation remains the foundation of AF ablation, but every experienced ablationist knows that some patients have triggers from the posterior wall, superior vena cava, crista terminalis, coronary sinus, left atrial appendage, mitral annular region, septum, or other atrial structures.
Niraj Sharma:The debate is not whether non PV triggers exist. The debate is whether we should routinely look for them during a first time AF ablation, how aggressively we should provoke them, and whether they are clinically meaningful or just lab noise. Orey and colleagues studied this using the University of Pennsylvania AF Registry. They included more than two thousand three hundred first time RFAF ablation patients who had successful PV isolation and underwent trigger provocative maneuvers. Provocation included cardioversion, isoproterenol up to twenty-thirty mcgmin as tolerated, and atrial burst pacing.
Niraj Sharma:Patients were divided into three groups: no non PV trigger, non PV trigger found and ablated, and non PV trigger found but untreated or not successfully eliminated. The result is memorable: one year recurrence was about thirty percent with no non PV trigger, thirty eight percent when a trigger was found and ablated, and seventy two percent when a trigger was found but not treated. That is where the statistics become clinically useful. An adjusted hazard ratio of about 3.7 for untreated triggers means these patients had nearly four times the hazard of recurrent AF or atrial tachycardia compared with patients without non PV triggers. The absolute difference was also large, more than 40 percentage points.
Niraj Sharma:That is not subtle. But even ablated triggers carried a worse prognosis than no triggers at all. That means the trigger is both a target and a marker. It may be something we should treat, but it also tells us the atrium has moved beyond PV only disease. Limitations matter.
Niraj Sharma:This was not randomized. The untreated group was small. It was a single expert center, and follow-up was not continuous for every patient. The EP Edge take, non PV triggers deserve respect. A reproducible trigger that initiates AF under isoproterenol, Pacing or spontaneous observation is not just a curiosity.
Niraj Sharma:In practice, this supports a more structured trigger strategy, especially in patients whose phenotype already suggests more advanced atrial disease. The next study is a nice counterbalance to all the technology we just discussed. It asks whether a very low tech intervention can help detect AF or atrial flutter. We live in a world of smartwatches, patches, handheld ECG devices, and implantable monitors. All of those have a role, but they also bring issues of cost, access, adherence, false positives, and detection of very brief episodes whose clinical meaning may be uncertain.
Niraj Sharma:So Chilkat et al. Asked a simple question: If high risk patients are taught to check their pulse for irregularity, will more AF or atrial flutter be diagnosed? It's important to note that this was a research letter published in JAC EP. So what's a research letter? It's a highly focused, concise report of original data.
Niraj Sharma:It is a peer reviewed article. It presents early or preliminary findings, novel methodologies or clinical observations that warrant rapid dissemination. With that background, this was a pilot randomized trial from the University of North Carolina Health System. Patients had elevated CHADS VASc scores and no known AF or flutter. They were recruited through the electronic health record portal.
Niraj Sharma:Four eighty four patients consented and were randomized to usual care or a pulse self exam intervention. The intervention was simple: a ninety second video teaching radial or carotid pulse assessment. Patients were asked to check twice daily for at least fourteen days. If they felt irregularity, they were told to contact their primary care provider for confirmatory testing. At one year, AF or flutter diagnosis was higher in the intervention group: five point nine percent versus two point two percent.
Niraj Sharma:The odds ratio was about two point nine. In plain language, the intervention nearly tripled the odds of diagnosis, although the confidence interval was wide, which tells us this was a pilot signal rather than definitive proof. The absolute difference was about three point seven percentage points. Practically that means roughly twenty seven high risk patients would need to receive the intervention to identify one additional diagnosis over a year, assuming the effect is causal. Anticoagulation was started numerically earlier in the intervention group, but that was not statistically significant.
Niraj Sharma:That distinction matters. Detection is only the first step. Stroke prevention requires confirmation, risk assessment, treatment, follow through. Limitations include low recruitment, selection of digitally engaged patients, no formal test of pulse check skill, provider dependent confirmatory testing, and reliance on EHR coding. The EP Edge take: Scalable medicine does not always need to be high-tech.
Niraj Sharma:Pulse self exam will not replace ECG confirmation or wearable monitoring, but it may fit into a tiered screening strategy: broad awareness first, confirmatory rhythm testing second, and longer monitoring for selected high risk patients. Now we move into left atrial appendage occlusion. The first paper is Veritas, studying the next generation Amulet three sixty device, with the accompanying editorial asking whether this gets us closer to freedom from anticoagulation. The story here is device evolution. The amulet concept has always been attractive because of its dual seal design a lobe to fill the appendage and a disc to seal the ostium but prior amulet experience also raised concerns about pericardial effusion, device embolization, and procedure related complications.
Niraj Sharma:So the rationale for Veritas was very specific: can a redesign preserve the seal while improving safety? The Amulet three sixty incorporated changes such as a more conformable distal lobe, an inverted distal end screw, modified stabilizing anchors, and an additional row of anchors. The goal was to keep the device stable and sealed, but reduce traumatic interaction with the appendage wall and adjacent structures. Veritas was a global, prospective, multicenter, single arm pre market study. It included 400 patients at 34 global sites.
Niraj Sharma:These were non valvular AF patients with elevated stroke risk, and a rationale to seek a non pharmacologic alternative to long term anticoagulation. Operators were experienced, and the main outcomes were early safety and forty five day TEE sealing. The early results were impressive. Implant success was ninety nine point eight percent. The primary safety endpoint was zero percent.
Niraj Sharma:The primary effectiveness endpoint, defined as leak of five millimeters or less at forty five days, was met in all evaluable patients. Complete closure was seen in about ninety four percent and no patient had a leak greater than three millimeters. But here is the statistical translation: zero events does not mean zero risk. The upper confidence limit was about zero point seven five percent, meaning the true event rate could still be below one percent, but not literally zero. Also, a perfect early ceiling endpoint does not yet prove long term stroke prevention.
Niraj Sharma:Device related thrombus was detected by the core lab in about two point four percent. That is important because core lab detection appeared more sensitive than site recognition. Limitations are clear: single arm design, selected anatomy, highly experienced operators, and only short term follow-up. The EP Edge take: Veritas is encouraging because it suggests device design matters, but left atrial appendage occlusion is ultimately judged by stroke prevention, bleeding reduction, pericardial safety, DRT management, and freedom from long term anticoagulation. Veritas is a strong early signal, not the final answer.
Niraj Sharma:The next left appendage occlusion paper takes us from a controlled pre market study to post market safety surveillance. Pericardial effusion is one of the most feared serious complications after left atrial appendage occlusion. Acute effusions are expected to be recognized around the procedure, but delayed effusions are more unsettling. The patient may have left the hospital, the implant may have looked successful, and then days or weeks later the patient presents with chest pain, dyspnea, dizziness, hypotension, or nonspecific decline. LeMay et al.
Niraj Sharma:Used the FDA MOD database to examine reported pericardial effusions after Watchman and Amulet devices. This is a passive adverse event reporting system. That means it is useful for signals, but it cannot give us reliable incidence rates. The investigators searched reports from each device's FDA approval through December 2024. Reports were included if they described pericardial effusion.
Niraj Sharma:Effusions were classified as acute if they occurred in hospital and late if they occurred after discharge. Among amulet reports, there were two ninety pericardial effusions. About two thirds were acute, but about one third were late presenting. More than half of the late amulet effusion reports required intervention, and mortality in reported amulet effusion cases was about eight percent in both acute and late groups. For WATCHMAN, there were fewer reported effusions in this database, and most were acute.
Niraj Sharma:But the most important statistical point is what we cannot say. These are not incidence rates. MOD does not provide the denominator of all implants, and reporting is incomplete, biased towards severe events, and potentially duplicative. So the correct interpretation is not a simplistic device comparison. The correct interpretation is vigilance.
Niraj Sharma:Late pericardial effusion after left atrial appendage occlusion is real, potentially serious, and should remain on the differential after discharge. The limitations are major: passive reporting, no denominator, variable report detail, market share differences, approval date differences, and no ability to prove mechanism. The EP Edge Take. This is not a device incidence paper. It is a safety awareness paper.
Niraj Sharma:In practice, it supports careful pre procedural CT anatomy, thoughtful sizing, awareness of pulmonary artery proximity, minimizing traumatic recapture or repositioning, and educating patients about post discharge symptoms. Left atrial appendage occlusion safety needs anatomy, not just event reporting. The next left atrial appendage occlusion paper asks a deceptively simple imaging question: where do peri device leaks actually live? Historically, we have talked about peri device leak mainly by size. Less than three millimeters, greater than three millimeters, greater than five millimeters, but location may matter.
Niraj Sharma:A posterior gap may not mean the same thing as an anterior gap or a through face leak. Device apposition depends on appendage shape, osteal ellipticity, ridge anatomy, deployment angle, and the mismatch between a circular device and an irregular appendage. Moteric et al. Studied WATCHMAN FLEX and FLEX PRO patients in a prospective multicenter registry with Core Lab imaging review. TEE was performed at implant and first follow-up and CT was performed at forty five-ninety days.
Niraj Sharma:Leaks on TEE were localized by region and leaks on CT were mapped using a clock face model. The key finding was that leaks were not randomly distributed. On post implant TEE, peri device leak was found in about seven percent and most small leaks were posterior. At follow-up TEE, about one quarter of patients had a leak, again most commonly posterior. Among larger follow-up TEE leaks, posterior location remained the most common.
Niraj Sharma:On CT, larger leaks clustered in the inferior posterior region, with the 07:00 location standing out. This is not an outcome study, so we should not overstate it. It does not prove that posterior leaks carry more stroke risk, more DRT risk, or require different treatment, but it does tell us that leak location has anatomy and that large leaks may cluster in a vulnerable zone. The limitations are important. The TEE and CT cohorts were not paired patient by patient.
Niraj Sharma:TEE and CT measure different things. TEE detects Doppler flow. CT detects contrast patency and anatomic gaps. Clinical outcomes were not captured, and this was focused on Watchman Flex and FlexPro. The EP Edge Take After left atrial appendage occlusion, the question should not only be how big is the leak, it should also be where is the leak and why is it there.
Niraj Sharma:For implanters, posterior and inferior posterior apposition deserve attention. For imagers, standardized localization may improve communication. For future devices, regional leak patterns may inform design. Now we come to one of the biggest questions in stroke prevention: left atrial appendage closure versus direct oral anticoagulants. For years, left atrial appendage closure was largely framed around patients who could not tolerate anticoagulation.
Niraj Sharma:But as procedural safety improves, the question has expanded: how does left atrial appendage closure compare with direct oral anticoagulant itself? This question is not one dimensional. Direct oral anticoagulants are effective, familiar and reversible, but bleeding risk, adherence, renal dysfunction, drug interactions, falls, cost, and patient preference matter. Left atrial appendage closure is a one time procedure, but it brings procedural risk, device related thrombus, peri device leak, post implant antithrombotic complexity, and possible residual ischemic stroke risk. Chan et al.
Niraj Sharma:Performed an updated meta analysis of randomized trials comparing percutaneous left atrial appendage closure with direct oral anticoagulant therapy in AF. They included four trials: PROG-seventeen Option, Closure AF, and CHAMPION AF. In total, there were five thousand eight hundred and ninety patients with median follow-up ranging from thirty six to forty two months. The results are best understood as trade offs. There was no statistically significant difference in all stroke, hemorrhagic stroke, systemic embolism, all cause death, or cardiovascular death.
Niraj Sharma:But ischemic stroke moved in the wrong direction for left atrial appendage closure. The relative risk was one point three six, with a p value of 0.06. That is not conventionally statistically significant, but it is close and clinically relevant. When the option trial was excluded, the ischemic stroke signal became statistically significant, with a relative risk of one point four five. Bleeding, on the other hand, favored left atrial appendage closure for non procedure related bleeding.
Niraj Sharma:Non procedure related major bleeding was reduced by about twenty one percent. Non procedure related non major bleeding was reduced by about fifty three percent. All non major bleeding was also reduced, but all major bleeding and intracranial hemorrhage were not significantly different. So what do the statistics mean? This is not left atrial appendage closure wins or direct oral anticoagulant win.
Niraj Sharma:This is phenotype selection. Left atrial appendage closure reduces long term non procedure related bleeding exposure but may carry a possible ischemic stroke trade off, depending on the population and trial mix. Limitations include different trial populations, different antithrombotic regimens, device evolution, and the use of pooled relative risks from event counts rather than harmonized time to event estimates. The EP Edge take: This is shared decision making evidence. For a patient dominated by bleeding risk, adherence problems, or true anticoagulant intolerance, left atrial appendage closure may be compelling.
Niraj Sharma:For a patient where ischemic stroke protection is the overriding priority and bleeding risk is acceptable, direct oral anticoagulant therapy may remain preferable. Finally, we move to conduction system pacing and a very practical LBBAP question: Once you have conduction system capture, does the exact lead position still matter? LBBAP has become a major part of physiologic pacing, but the LBB area is not one tiny target. It includes true LBB capture, fascicular capture, and in some cases deep septal myocardial capture without definite conduction system capture. The rationale for the Martinez study was simple: should operators chase a more central left bundle capture site, or is proving conduction system capture enough, at least in preserved ejection fraction patients?
Niraj Sharma:The authors used myocardial work analysis because QRS duration alone may not tell the entire mechanical story. Myocardial work combines strain imaging with blood pressure to estimate left ventricular performance, including global work efficiency, constructive work, and wasted work. This was a prospective single center cohort of one hundred and fourteen patients with preserved ejection fraction undergoing LBB pacing for bradycardia indications. All had confirmed conduction system capture. Patients were categorized as central capture, meaning left bundle trunk or septal fascicular pacing, or peripheral capture, meaning posterior or anterior fascicular pacing.
Niraj Sharma:Echocardiography and myocardial work were assessed at follow-up roughly eighteen months later. The main result was neutral. Global work efficiency was about 88.6% with central capture and 89% with peripheral capture. The mean difference was only about -0.4 percentage point and the p value was 0.626. Other measures, including global longitudinal strain, interventricular mechanical delay, peak strain dispersion, global work index, constructive work, and wasted work were also similar.
Niraj Sharma:The paired intrinsic versus paced analysis was also reassuring. In patients with intrinsic rhythm available, LBB pacing did not produce a major deterioration in global mechanical efficiency compared with intrinsic activation. But the editorial is exactly right to urge caution. This does not prove lead position never matters. Only ten patients had true left bundle trunk pacing.
Niraj Sharma:The study mostly compared septal fascicular capture with posterior fascicular capture. The cohort had preserved ejection fraction and mostly bradycardia indications, not LBBB cardiomyopathy or CRT indications. The EP Edge take: For preserved EF bradycardia patients, proven conduction system capture may matter more than chasing an ideal coordinate, but in resynchronization patients the question remains open, and an RR' pattern in V1 alone is not enough. Good LBBAP pacing requires physiologic evidence, capture transitions when available, V six R wave peak time, paced morphology, intracardiac signals, threshold behavior, lead depth, stability, and the clinical reason for pacing. Let us bring this issue together.
Niraj Sharma:PFA is moving from energy source to infrastructure. Faster procedures, higher lab capacity, new device designs, and a need for smarter safety surveillance. AF ablation is moving beyond a PV only reflex, with non PV triggers acting as both targets and markers, while even pulse self exam reminds us that good screening does not always need expensive technology. Left atrial appendage occlusion is entering a more demanding evidence era. Excellent early sealing is not the same as long term stroke prevention, pericardial effusion can be late, leak location matters, and left atrial appendage closure versus direct oral anticoagulation therapy is best understood as a trade off between bleeding reduction and possible ischemic stroke signal, and in LBBAP, the message is precision with humility.
Niraj Sharma:Capture matters, but phenotype may determine how much lead position matters. For full details, exact statistics, references, and graphics, please go to the LinkedIn newsletter EP Edge Journal Watch and to Substack at epedge.substack.com. Questions, suggestions or concerns can be emailed to epedge. Castgmail . com. Thank you again for listening to EP Edge Journal Watch.
Niraj Sharma:I appreciate your time, your feedback and your commitment to thoughtful electrophysiology. Take care, and I will see you in the next episode.