Niraj Sharma: Welcome back to EP Edge Journal Watch. I am Doctor. Sharma and I am grateful you are here. If you have been listening regularly, sharing episodes or sending feedback, thank you. I know your time is valuable and it means a lot that you choose to spend a few minutes with me each week.
Alright, let's get into today's journal watch. Here's what we'll cover: one. Those almost AF runs: irregular atrial arrhythmias that are under thirty seconds. Do they matter? Or are they noise?
Two. Metabolic modulation, specifically semaglutide, used around the time of ablation in patients with obesity and paroxysmal atrial fibrillation. Does it meaningfully change recurrence and arrhythmia burden? Nanosecond pulse field ablation for paroxysmal atrial fibrillation, twelve month outcomes, and a workflow that leans heavily toward conscious sedation. Fourth, a high stakes safety signal: generalized coronary spasm in Marshallese patients after pulse field ablation, rare globally, potentially common locally, and potentially catastrophic.
Fifth, implantable loop recorder accuracy: how often alerts are true, how often they are false, and how much the vendor matters. Sixth, practical intra procedural safety cues for left bundle branch area pacing: distinct electrogram waveforms that flag septal perforation. Seventh, validation of the PADIT risk score for device infection. And an important twist pocket infection and systemic infection behave differently. And eighth, polycystic ovarian syndrome and long term risk of arrhythmias, including atrial arrhythmias, conduction disease, and even device implantation over decades.
Okay, let's start with the shortest episodes that can create the biggest clinical uncertainty. Study one asks a deceptively simple question: If you see an irregular atrial arrhythmia that looks like atrial fibrillation but is under thirty seconds, does that predict that the patient will declare true atrial fibrillation later on the same monitoring period? The clinical context matters here. Our diagnostic threshold in ambulatory electrocardiography has been anchored to the thirty second rule. But in the real world people have shorter atrial fibrillation like bursts all the time.
So the question is not do we anticoagulate a six second episode? The question is should that six second episode change what we do next? This analysis used thirty day continuous ambulatory electrocardiography data over thirty two thousand United States patients with full disclosure monitoring and technician verification of events. They focused on irregular supraventricular episodes without clear P waves that would have been called atrial fibrillation if they lasted longer. Here is the key signal: in the final cohort, early ultrashort episodes under thirty seconds were uncommon, under one percent, but when they happened, the risk enrichment was dramatic.
Nearly half of those patients went on to have atrial fibrillation lasting at least thirty seconds during the same monitoring window. Statistically, the hazard ratio for progressing to atrial fibrillation lasting at least thirty seconds was a little over eight. That is not subtle. Now let's interpret that carefully. This does not mean we should relabel every short run as atrial fibrillation and start treatment reflexively.
What it does mean is that an early atrial fibrillation like burst under thirty seconds can be a high signal to noise marker that the patient is about to declare longer atrial fibrillation. So what do you do Monday morning with this? Think of this as a trigger for escalation of ascertainment. If downstream decisions depend on confirming atrial fibrillation, especially in a patient with meaningful stroke risk, This is the kind of finding that should push you toward longer monitoring, not reassurance. They do not have granular clinical risk information like stroke risk variables, and the rarity of early ultrashort episodes means this is a small subgroup even in a big dataset.
But the directionality is hard to ignore. Ultrashort does not necessarily mean unimportant. Okay, now let's move from signal detection to substrate modification. Study two lies at the intersection of electrophysiology and metabolism. We all know obesity increases atrial fibrillation recurrence after ablation.
We also know glucagon like peptide, one receptor agonist like semaglutide, can produce meaningful weight loss. The real question is does that translate into less atrial tachyarrhythmia recurrence after ablation? This was a single center propensity matched cohort of patients with obesity undergoing first time ablation for paroxysmal atrial fibrillation. Semaglutide was started either shortly before ablation or shortly after. And here is an important strength: rhythm surveillance used implantable cardiac monitors, so they are not guessing based on symptoms alone.
The matched groups were 181 versus 181. At a median follow-up of about eighteen months, freedom from recurrence was roughly eighty percent with semaglutide versus about sixty five percent without. The hazard ratio for recurrence was about half so a meaningful association. And they did not just report time to first recurrence, they also saw a lower atrial tachyarrhythmia burden over time in the semaglutide group. Weight loss was not trivial here.
The semaglutide group lost on the order of 10 plus kilograms on average, with a meaningful body mass index reduction compared with very small changes in controls. Procedurally, energy sources were balanced and major adverse events like death or stroke were not seen in either group. So what is the clinical implication? The authors introduce an idea that I think is strategically important: a periablation therapeutic window for metabolic conditioning. In other words, rhythm control is not purely an ablation only solution.
It can be an integrated electrophysiology metabolic intervention. But we need to be honest about causality. Propensity matching helps balance measured variables, but it does not eliminate selection effects. Access, adherence, clinician selection, and calendar time bias can all creep in. So I take this as a strong hypothesis with supportive evidence, not as a final answer.
Practical takeaway: If you are ablating atrial fibrillation in patients with obesity, This paper supports being more intentional about structured metabolic therapy around the procedure, and it reinforces that continuous monitoring is the right way to measure true arrhythmia burden when you are making these claims. Next, pulse field ablation, but in the nanosecond domain and with workflow implications that could change lab throughput. Study three is SINA AF, High Repetition Frequency Nanosecond Pulse Field Ablation for Paroxysmal Atrial Fibrillation. The concept is appealing: nanosecond pulse paradigms may reduce neuromuscular stimulation, which could enable more cases under local anesthesia and conscious sedation, without sacrificing lesion efficacy. This was a prospective multicenter single arm study across 11 centers enrolling symptomatic drug refractory paroxysmal atrial fibrillation patients.
They performed pulmonary vein isolation using a commercial nanosecond pulse field system. The primary efficacy endpoint was freedom from atrial fibrillation, atrial flutter, or atrial tachycardia lasting at least thirty seconds from day ninety one through day three sixty five of class I or class III antiarrhythmic drugs. Acute pulmonary vein isolation success was one hundred percent. At twelve months, the primary efficacy estimate was about eighty eight percent. On safety: no device or procedure related death, stroke, or transient ischemic attack.
Serious adverse events were limited to minor vascular complications that resolved without sequelae. Now the workflow piece. This is the part many labs will focus on. Over ninety percent of cases were performed under local anesthesia with conscious sedation. General anesthesia was used in a small minority.
If you are trying to scale atrial fibrillation ablation capacity, that matters because anesthesia resources can be a bottleneck. But here is the key interpretive caution: Monitoring intensity was not continuous implantable monitoring. Intermittent electrocardiography and symptom driven reporting can underestimate asymptomatic recurrence, so treat the efficacy number as freedom from detected recurrence, not necessarily freedom from recurrence. Clinical implication: This is a clean feasibility and performance signal. Nanosecond pulse field ablation can deliver strong twelve month outcomes in paroxysmal atrial fibrillation with a sedation profile that could materially change throughput and operational planning.
The next step is comparative trials with rigorous, ideally continuous monitoring. Now let's pivot to a safety signal that demands attention, especially because it may be population enriched. Study four is the kind of report that can change practice faster than a randomized trial because the downside risk is so high. This is a retrospective single center cohort of patients of Marshallese descent undergoing atrial fibrillation ablation comparing pulse field ablation with thermal ablation. The cohort is small, 12 total patients, so we have to keep our statistical humility.
But the signal is extreme. Every pulse field ablation patient in this series experienced generalized coronary spasm, and none of the thermal ablation patients did. The clinical presentations range from transient intra procedural ischemia, responsive to intravenous nitroglycerin, all the way to delayed ischemia with ventricular fibrillation or bradycardic shock requiring vasopressors, nitroglycerin, intravenous or intracoronary, and even mechanical circulatory support. And notably, events occurred despite no pulse field energy delivery near the coronary arteries. So what do we do with this?
This is not a paper about mechanism certainty. It is a paper about operational readiness and risk awareness. The authors emphasize delayed presentations and life threatening potential that has immediate implications for post procedure monitoring strategy and same day discharge assumptions. Let me say that plainly: if a population truly has a higher susceptibility to generalized spasm after pulse field ablation, then standard pathways may not generalize. Observation time, discharge planning, and readiness to treat spasm may need to be population aware.
Limitations are obvious: small sample size, non randomized comparison, and potential temporal confounding. But the severity of events makes this difficult to ignore. This is a rare globally common locally warning signal and electrophysiology ignores those at its peril. Next, how reliable are the implantable loop recorder alerts that increasingly drive both clinical workload and trial endpoints. Study five is extremely practical: implantable loop recorder accuracy across vendors, because implantable loop recorders are now everywhere.
Stroke evaluation, syncope, palpitations, atrial fibrillation management, and their alerts can quietly create two major problems: clinic workload explosion and distorted atrial fibrillation burden endpoints in research. This was a multicenter, multi vendor remote monitoring database, including hundreds of thousands of electrocardiogram available episodes from thousands of patients. They focused on alert events, So these are the transmissions that actually hit your inbox. And physicians adjudicated true versus false. Key result number one: Overall true positives versus false positives were roughly fiftyfifty.
Key result number two: Vendor differences were large. For atrial tachycardia and atrial fibrillation alerts, positive predictive value, meaning the fraction of alerts that were truly atrial fibrillation, was about seventy three percent for Boston Scientific, about fifty six percent for Medtronic, about fifty one percent for Abbott, and about twenty three percent for BioTronic, And false positives were not evenly distributed. In BioTronic, false positives were often driven by ectopy. For tachycardia alerts, false positive rates were also high in some vendors. Now the most important nuance, positive predictive value is not sensitivity.
This study could not quantify false negatives, and that matters for high stakes indications like post stroke atrial fibrillation detection. But positive predictive value is what drives decision noise and, workload. If your device generates five alerts and half are false, your clinical team pays for that in time, and your patient pays for it in anxiety and downstream testing. Clinical implications are immediate: one. Implantable loop recorder alerts are not interchangeable across vendors.
Two. Atrial fibrillation burden derived from alerts may partly reflect vendor algorithms and programming choices, not just patient substrate. So if you are using implantable loop recorder burden as an endpoint, whether clinically or in trials, build adjudication and vendor awareness into your interpretation. Now let's move into the procedure room for a different kind of signal: electrogram based detection of septal perforation during left bundle branch area pacing. Study six tackles a complication we all worry about in conduction system pacing programs: septal perforation during left bundle branch area pacing implantation.
The classic marker many of us use is a drop in current of injury amplitude, but this paper asks can we do better by treating the intracardiac electrogram as a waveform phenotype, not just a single number? They evaluated consecutive cases with perforation and analyzed intracardiac electrograms, both filtered and unfiltered, along with current of injury measurements. They also proposed a practical definition for microperforation combining low sense current of injury, impedance drop, and capture characteristics. The baseline finding is strong and intuitive. Sense current of injury amplitude during perforation was dramatically lower than at the final position.
But here's where the paper becomes operationally useful. They show that baseline electrocardiogram phenotype matters. In patients with a narrow QRS complex and no left bundle branch block, a specific rule performed well. If the Q or S wave amplitude is greater than the current of injury amplitude, that pattern had high sensitivity and high specificity for perforation. And that matters because it gives you a bedside rule you can teach, standardize and audit, especially for teams scaling left bundle branch area pacing volume.
The authors also point out a practical workflow nuance: intermittently interrupt pacing, so you can analyze sensed waveforms when the paced current of injury starts trending down toward concerning values. My takeaway is simple: Perforation detection should not be a single scalar threshold. It should be a waveform based pattern recognition skill, conditioned by baseline activation pattern. That's the level a nuanced conduction system pacing program should build into training and recording protocols. Device infection risk: why the subtype matters and how PADET trial performs when you split pocket from systemic infection.
Study seven looks at device infections and the PADET score which used five criteria which were: Prior procedure, age, depressed renal function, immunosuppressed state, and complexity of procedure. The interpretation: Low risk: zero-four points Intermediate: five-six points and High risk: equal to or greater than seven points. This trial attempts to validate the PADET risk score for infection after cardiac implantable electronic device procedures and then goes a step further by separating pocket infection from systemic infection. This matters because device infection is not a single biological entity. Pocket infection often reflects local barrier disruption and cumulative pocket manipulation.
Systemic infection behaves differently: more bloodstream dynamics, more lead related biology, and often a different procedural trigger. This was a large prospective registry at a single institute, covering all device procedures over many years with adjudicated infection outcomes. The primary outcome was hospitalization for device infection, subclassified into pocket versus systemic infection. Overall infection was under one percent, with pocket infections making up the majority. In terms of model performance, the PADET score was moderately discriminative overall, but the real insight is in the subtype divergence.
They found that prior procedures were strongly associated with pocket infection but not systemic infection, and systemic infection risk showed particularly strong association with lead revision and complex device types. So the practical message is not just higher score means higher risk. The message is prevention strategies should be phenotype aware. Pocket infection risk should push you to think about pocket biology and cumulative perturbation, while systemic infection risk should push you to think about procedural complexity, lead handling, and the specific vulnerability created by revisions. Okay, last study: a women's cardiovascular health signal that spans atrial arrhythmias, conduction disease, and device implantation over long follow-up.
Study eight evaluates polycystic ovarian syndrome and long term risk of arrhythmias. This is important because polycystic ovarian syndrome is metabolically complex, and prior outcome data connecting it to arrhythmias has been limited. This study used a nationwide Danish cohort with over twenty six thousand patients with polycystic ovarian syndrome matched to controls and followed for years, through early twenty twenty four. They examined a broad set of outcomes: atrial arrhythmias, conduction disease, cardiac arrest, and even device implantation. The signal they report is an elevated associated risk of incident arrhythmias over time.
Importantly, it is not just one rhythm category. It spans atrial fibrillation and flutter, conduction disease requiring devices, and hard outcomes. They also report a higher incidence of cardiac implantable electronic device implantation, with an adjusted hazard ratio meaningfully above one. Now limitations are real, diagnosis coding is not perfect, and they do not have deep phenotype granularity like body mass index, adiposity, smoking, and other metabolic variables. Surveillance bias is possible.
Patients with polycystic ovarian syndrome may interface with healthcare more, which can raise detection. But even with those caveats, the clinical implication is worth taking seriously. Polycystic ovarian syndrome may flag a broad electrophysiologic vulnerability over decades, not just a single arrhythmia endpoint. That should influence how we think about long horizon risk in women's cardiovascular health, particularly when metabolic features are present. Let me close by pulling the whole issue together: one.
Ultrashort atrial fibrillation like episodes under thirty seconds can be powerful risk enrichment markers, often a reason to intensify monitoring, not dismiss it. Two. Semaglutide around ablation is associated with lower recurrence and lower burden under continuous monitoring, but we still need randomized confirmation. Three. Nanosecond pulse field ablation shows strong twelve month outcomes and a sedation profile that could change lab workflow, but monitoring intensity remains a key limitation.
Four. Generalized coronary spasm in Marshallese patients after pulse field ablation is a high stakes safety signal that should influence operational planning and post procedure monitoring. Five. Implantable loop recorder alerts vary widely by vendor. What you call burden may partly be algorithm and programming, not just biology.
Six. In left bundle branch area pacing, perforation detection improves when we interpret electrograms as phenotype, not just current of injury amplitude. Seven. PADD it is more useful when you respect infection subtype biology, not just a single pooled outcome. Eight.
Polycystic ovarian syndrome appears linked to a broad arrhythmia and device implantation phenotype over long follow-up. As always, the full newsletter with references and graphics is available on the LinkedIn newsletter and also on Substack at epedge.substack.com. If you have questions, comments or suggestions you can reach me at epedgecastgmail .com. Thank you again for listening and for supporting EP Edge Journal Watch. Until we meet again, take care.