Disclaimer: 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 thank you for joining me for Issue 21, May 2026. This is a packed issue. We are going to start with AI guided redo ablation for atrial fibrillation, specifically in the challenging patient whose pulmonary veins are already isolated.
Then we will move into dual energy lattice tip ablation for ventricular arrhythmias and a very important safety cluster around pulsed field ablation and cardiac implantable electronic devices. We will also cover neuromodulation for PVCs, cannabis and atrial arrhythmias, sudden death risk after hypertrophic cardiomyopathy myectomy, atrial fibrillation as a possible ventricular arrhythmia risk marker in heart failure with preserved EF, a simple ECG clue for pacemaker risk in right bundle branch block, and finally the evolving evidence around anticoagulation after apparently successful AF ablation. The thread running through this issue is simple. New tools are giving us new options but they also require better judgment about patient selection, monitoring and safety boundaries. So let's get started.
Our first study is the RESEART trial. This was a study of redo AF ablation in patients whose pulmonary veins were already isolated. That is the key clinical problem here. If a patient comes back with recurrent symptomatic AF and the veins have reconnected, the strategy is straightforward: re isolate the veins. But if the veins are still isolated, the question becomes much harder: Where exactly do you ablate?
Tested whether artificial intelligence guided detection of spatiotemporal electrogram dispersion could identify functional non PV substrate in this durable PVI redo population. This was a prospective interventional multicenter single arm trial. Patients had prior catheter or surgical ablation for AF and had symptomatic recurrent AF. Importantly, if pulmonary vein reconnection was found during the procedure, the patient was withdrawn from the trial. So this was really focused on the durable PVI recurrence phenotype.
The operators used Volta AF Explorer to identify dispersion regions in both atria, and then ablated those dispersion areas with radiofrequency energy. Empirical anatomic lines were not allowed. Follow-up included visits at three, six and 12, with ECG and at least twenty four hour Holter monitoring unless the patient had an implantable device. The primary endpoint was freedom from documented AF at twelve months after a single AI guided repeat ablation procedure. Now let's talk about the numbers.
A total of two thirteen patients were enrolled. The main reasons for premature study exit were pulmonary vein reconnection in eighty patients and non inducibility of AF in fourteen patients. Ninety six patients underwent a successful Index AI guided procedure and ninety three were included in the intention to treat analysis. Freedom from documented AF at twelve months was eighty three percent or seventy seven out of ninety three patients. The ninety five percent confidence interval was seventy four percent to eighty nine percent.
That confidence interval means that based on this sample, the likely true estimate is somewhere in that range. It is a strong signal, but it is still a single arm study. Freedom from any atrial arrhythmia after one procedure was seventy percent, with a ninety five percent confidence interval from sixty percent to seventy eight percent. AF termination during ablation occurred in fifty four percent of patients and right atrial dispersion was identified in fifty nine percent. Quality of life improved as well.
The Affect overall score increased from 66.1 to 85.8, with a p value less than 0.0001. That p value tells us the improvement was very unlikely to be due to chance alone. Procedure related serious adverse events occurred in six of ninety six patients, or about six percent. So what is the EP Edge take? Restart is interesting because it studies the exact redo case that frustrates us in practice.
If the veins are still isolated, simply repeating PVI is not a strategy. The eighty three percent freedom from AF signal is impressive, but without a randomized comparator, we should not oversell it. In practice, I would view dispersion mapping as a disciplined way to find targets in durable PVI recurrence. I would not yet view it as proof that AI guided ablation is superior to every other redo approach. For now, this is promising, practical, and worth watching closely.
The second paper is ClearVT. This is the early U. S. Experience with catheter ablation of ventricular arrhythmias using a dual energy lattice tip catheter. The clinical context is scar related VT ablation, which remains difficult.
Lesion size matters, irrigation burden matters, intramural substrate matters, catheter stability matters, procedure time matters. The dual energy lattice tip catheter is attractive because it has a larger footprint and can deliver both radiofrequency ablation and pulsed field ablation, but ventricular arrhythmia ablation is a much more demanding environment than AF ablation. Clear VT came from the prospectively maintained Cleveland Clinic VT registry. Patients treated with the SPHER-nine lattice tip RFPFA catheter from January to September 2025 were analyzed. There were fifty nine patients in total, fifty had scar related VT and nine had frequent PVCs.
The catheter was selected for patients with extensive target substrate or prior failure of conventional radiofrequency ablation. In general, radiofrequency was used first. Pulsed field ablation was used as an adjunct, mainly in dense scar with wall thinning or absent contractility on intracardiac echo and low bipolar voltage. The endpoints included clinical VT elimination, VT noninducibility, abnormal electrogram elimination, and PVC suppression. Now the results.
The median age was around 70 years and mean LVEF was thirty six point three percent. Among the VT patients, forty percent presented with electrical storm, thirty percent had prior VT ablation, sixty eight percent had recurrent VT despite amiodarone. So this was not a simple population. Acute VT non inducibility was achieved in seventy eight percent. Clinical VT elimination and abnormal electrogram elimination were achieved in all VT cases.
For the PVC group, acute PVC suppression was achieved in one hundred percent. PVC burden decreased from twenty point four percent to three point five percent after ablation. At six months, Kaplan Meier estimated VT free survival was sixty nine point eight percent. Let me translate that. Kaplan Meier analysis estimates the probability of remaining free from VT over time, while accounting for patients who have different lengths of follow-up.
The fine grey cumulative incidence of VT recurrence was twenty eight point four percent after accounting for competing risks. That matters because in a very sick VT population, patients may die, receive an LVAD or undergo transplant before they can have recurrent VT. Fine gray analysis tries to account for those competing events. There were three major procedure related complications, including two major bleeding events and one CRTD generator failure after pulsed field ablation about 7.5 millimeters from an LV pacing lead. Another important point: PFA did not reliably create transmural effects in non ischemic septal substrate.
Contralateral abnormal electrograms persisted and required additional ablation. So what does the EP Edge take? ClearVT is not just another new technology paper. It shows why lattice tip ablation is attractive for large scar regions, but it also shows why powerful platforms need careful rules. The efficacy signal is encouraging, but the safety details are just as important: device interaction, valve entrapment, epicardial fat entrapment, steam pops, and incomplete septal transmurality.
I would not summarize this as bigger catheter, better ablation. The better summary is: powerful platform, useful tool, new safety playbook required. The third topic is the PFA and cardiac implantable electronic device or CIED Safety Cluster. This is one of the most practical sections in this issue. Pulsed field ablation has moved very quickly, but many pivotal trials did not include the patients we see every day.
Patients with pacemakers, ICDs, CRT systems, leadless pacemakers, abandoned leads, and complex lead anatomy. This group of reports makes the safety issue very concrete. There are several papers here. Nayer et al. Described cardiac implantable electronic device software reset and permanent generator damage after monopolar lattice tip Goldar et al.
Reported asynchronous PFA induced ventricular fibrillation in a patient with an ICD during right superior pulmonary vein ablation. Kovac et al. Reported recurrent ventricular fibrillation during lattice tip radiofrequency ablation near right ventricular ICD coils in VT ablation patients. Kipolla et al. Framed the device standards problem, pointing out that current CIED electromagnetic compatibility standards do not fully address modern ablation energy exposure.
Let's break down the signal. In the NIAIR report, one patient had irreversible CRT degenerator failure during SVC pulsed field ablation near an ICD coil. Another patient had an AVAIR atrial leadless pacemaker software reset with a transient battery life abnormality that later normalized. In the Golder report, ventricular fibrillation occurred immediately after PFA delivery in the right superior pulmonary vein. CT imaging showed that the right ventricular lead was less than one centimeter from the right superior pulmonary vein.
That supported a possible lead mediated myocardial capture mechanism, essentially a In the Covest report, ventricular fibrillation was reproducibly induced during lattice tip radiofrequency ablation near right ventricular ICD coils. Pectoral muscle contraction over the generator suggested that the ICD system have become part of the RF return pathway, and the device standards editorial made the broader point: Modern PFA waveforms and ablation current pathways may exceed what older device standards were designed to test. The practical implications are important: interrogate devices before and after ablation. Be especially careful when energy is delivered near leads, coils, leadless pacemakers, or generator connected conductors. Avoid direct or near direct contact between high energy ablation electrodes and ICD coils, exposed conductors, leadless devices, or other implanted hardware.
If the target is close to ICD coils or chronic lead hardware, consider using a different catheter or a different energy source. For PFA, synchronized delivery may matter, particularly near device leads, because asynchronous delivery can theoretically capture myocardium during the vulnerable period. Use fluoroscopy, ICE, or selective pre procedural imaging when planned lesions are close to SVC coils, RV coils, coronary venous leads, leadless devices, or left atrial appendage occlusion hardware. The EP Edge take is this: PFA is not automatically safe just because it is tissue selective. It is still an electrical therapy delivered in patients with conductors.
If the ablation catheter is near a lead, coil, leadless pacemaker or exposed conductor, I would treat the device system as part of the electrical environment. The practical steps are straightforward: know where the hardware is, avoid direct or near direct contact, use ice or fluoroscopy when needed, interrogate before and after, and be especially cautious with monopolar systems near coils. This is going to be an evolving area and I expect labeling, manufacturer guidance, HRS input and device standards to keep changing. Next is Treat PVC, along with the editorial titled When Sham Works. This was a randomized trial of transcutaneous electrical vagus nerve stimulation for PVC suppression.
The idea is appealing. PVCs can be autonomically influenced. Drug therapy is often unsatisfying. Ablation can be difficult depending on the origin, especially with papillary muscle PVCs, LV summit PVCs, epicardial origins that are not easily inducible. So the question was can low level tragga stimulation reduce PVC burden?
Treat PVC was a prospective multicenter, double blind, sham controlled randomized trial at seven tertiary centers in China. One hundred patients were randomized one to one to active low level tragus stimulation at the tragus or sham stimulation at the earlobe. Ninety six patients were included in the final analysis. The stimulation protocol was 20 Hz, 0.2 ms pulse width, individualized intensity one mA below the discomfort threshold, and two thirty minute sessions daily for six months. The primary endpoint was change in PVC burden using ten day ambulatory ECG monitoring.
That is important because PVC burden can vary a lot day to day. A ten day monitor is much stronger than a single twenty four hour Holter for this type of trial. Secondary endpoints included heart rate variability, skin sympathetic nerve activity, inflammatory cytokines, adherence, quality of life, and adverse events. Now the results: PVC burden decreased in the active LLTS group from eighteen point seven percent to eleven point one percent at six months, with a p value less than 0.001. That sounds good, But the sham group also improved.
PVC burden decreased from sixteen point seven percent to twelve point six percent, also with a p value less than 0.001. When the two groups were compared against each other, there was no significant benefit of active stimulation. The p value for absolute reduction was 0.888 and the p value for relative reduction was 0.105. In simple terms, both groups improved but active tragus stimulation did not beat sham earlobe stimulation. Adherence was high and similar: eighty five point four percent in the active group and eighty nine point six percent in the sham group.
Heart rate variability shifted in both groups toward parasympathetic dominance, but there was no difference between groups. Skin sympathetic nerve activity and inflammatory markers also did not significantly differ. Adverse effects were minimal, mainly local auricular rash or redness. So what does the EP Edge take? This trial should not push low level tragal stimulation into routine PVC management.
It should make neuromodulation studies better. The active arm improved but the sham arm improved too. That is the whole lesson. For clinicians, I would not offer LLTS as an evidence based PVC therapy based on these data. For researchers, the message is even clearer.
In device based autonomic trials, placebo effects, PVC variability, and possibly active sham physiology must be built into the design from the beginning. A good mechanistic idea still has to beat a good sham. The next paper is about Cannabis use and atrial arrhythmias. This is a systematic review and meta analysis of large population studies. Cannabis use is common, increasingly normalized, and often left out of arrhythmia conversations.
For atrial fibrillation, atrial flutter, SVT, and atrial tachycardia, that omission is becoming harder to justify. The rationale was simple: Does recreational cannabis use associate with atrial arrhythmias across large epidemiologic datasets? This was a systematic review and random effects meta analysis of observational studies through April 2024. It was prospectively registered in PROSPERO. 14 observational studies were included, with more than 81,000,000 participants from North America, Europe, and Oceania.
The composite atrial arrhythmia outcome included AF, atrial flutter, atrial tachycardia, and SVT. Subgroup analyses looked at concomitant substance use, region, legalization status, and study design. Here are the key results: Cannabis users represented one point one percent of the total population. Atrial arrhythmias occurred in twelve point five percent of cannabis users versus two point seven percent of controls. Cannabis use was associated with increased atrial arrhythmia risk, with a pooled odds ratio of one point seven one.
Let me explain that. An odds ratio of one point seven one means the odds of atrial arrhythmia were seventy one percent higher in cannabis users compared with controls in the pooled analysis. The ninety five percent confidence interval was 1.13 to 2.58 and the p value was 0.012. Since the confidence interval does not cross one and the p value is below 0.05, this was statistically significant. Concomitant drug use showed a higher signal, with an odds ratio of one point nine one.
Isolated cannabis use still showed increased risk, with an odds ratio of one point three nine. Cannabis legal countries showed an odds ratio of one point nine three. But there is a very important limitation: heterogeneity was extremely high, with I2 around 99.75%. I2 tells us how much of the variation across studies is due to differences between studies rather than random chance. And I squared this high means the included studies were very different from each other.
So we should not over interpret this as a precise causal estimate. The evidence is observational. It cannot prove that cannabis causes AF in every exposed patient. Exposure definitions were inconsistent. ICD coded cannabis use may capture heavier or more medically visible use.
Dose, root, THC concentration, chronicity, synthetic cannabinoids, and adolescent data were limited. The EP Edge take is straightforward. This is a counseling paper. It gives us enough signal to stop treating cannabis as a harmless social history footnote. In patients with AF, flutter, SVT, unexplained palpitations, or early onset atrial arrhythmias, I would ask directly about cannabis.
Ask about route, frequency, dose, co use with alcohol or stimulants, and timing relative to symptoms. The right clinical message is measured, not moralizing. Cannabis may be arrhythmia relevant and patients should know that. Now let's move to hypertrophic cardiomyopathy. This study looked at predictors of sudden cardiac death in patients with obstructive hypertrophic cardiomyopathy or HCM after surgical septal myectomy.
The clinical point is important. Septal myectomy can relieve obstruction and improve symptoms, but it does not remove myocardial fibrosis, and fibrosis may continue to define residual arrhythmic risk even after the gradient is fixed. This was a retrospective cohort from FUI Hospital in Beijing. It included consecutive obstructive HCM patients undergoing surgical septal myectomy who had preoperative contrast enhanced cardiac MRI. The final cohort included thirteen eighty nine patients treated between 2008 and 2020.
The primary endpoint was sudden cardiac death or equivalent after myectomy. The authors used competing risk regression. That is important because in HCM patients can die from causes other than sudden death, and those events compete with the endpoint being studied. Now the results. The median age was 48, and thirty eight point nine percent were women.
Preoperative late gadolinium enhancement was present in eighty three point nine percent of patients. The median LGE extent was four point two eight percent of LV mass. Median follow-up was three point two nine years. All cause mortality occurred in forty patients or three point zero three percent. The primary endpoint occurred in sixteen patients or one point eight percent.
That included sudden cardiac death in eleven patients and aborted sudden death in five. Five year survival free from sudden cardiac death was ninety eight point five percent, with a ninety five percent confidence interval from ninety seven point six percent to ninety nine point five percent. So the absolute event rate was low, but the question is who remains at risk? Pre operative LGE extent remained independently associated with sudden death after competing risk adjustment. The subdistribution hazard ratio was 1.06 per percent LV mass, with a 95% confidence interval of 1.01 to 1.12 and a p value of 0.027.
In practical terms, each additional percent of LV mass with LGE was associated with a higher residual sudden death risk. History of sustained VT or VF was also strongly associated with sudden death risk. There are limitations. This was retrospective and single center. The number of sudden death events was small, which limits model stability.
Follow-up was relatively short for HCM risk prediction, and not every surgical patient underwent contrast CMR, which may introduce selection bias. The EP Edge take is clean. Myectomy changes obstruction, not scar. A good post myectomy gradient should not make us ignore preoperative LGE. This study supports keeping LGE extent in the ICD and surveillance conversation after myectomy, especially when LGE is extensive or when there is prior sustained VT or VF.
I would not use this paper to create a rigid new ICD threshold. I would use it to avoid false reassurance. The next study asks whether atrial fibrillation is associated with ventricular tachyarrhythmias or cardiac arrest in heart failure with preserved ejection fraction. Heart failure with preserved EF has a sudden death problem, but we do not have the same practical risk framework that exists for reduced ejection fraction. AF is common in heart failure with preserved EF.
This paper asks whether AF marks a higher risk ventricular arrhythmia phenotype. This was a single center retrospective cohort from a cardiac specialty hospital. It included nine fifty one patients diagnosed with heart failure with preserved EF between 2015 and 2022. All had LVEF at least fifty percent. Clinical variables and outcomes were derived from electronic health record diagnosis codes.
The authors used backward stepwise multivariable logistic regression to evaluate associations with ventricular tachyarrhythmias or cardiac arrest. The results were interesting. Mean age was 73.5 years and fifty two percent were women. Coronary artery disease was present in seventy five percent and atrial fibrillation was present in forty nine percent. Ventricular tachyarrhythmia or cardiac arrest occurred in forty six patients or five percent.
AF was independently associated with VTA or cardiac arrest, with an odds ratio of four point one two. The 95% confidence interval was 2.01-8.41, and the p value was less than 0.0001, so statistically, this is a strong association. An odds ratio of four point one two means the odds of ventricular tachyarrhythmia or cardiac arrest were about four times higher in heart failure with preserved EF patients with AF compared with those without AF after adjustment in the model. Coronary disease, male sex, and chronic kidney disease entered the model, but their confidence intervals crossed unity. In other words, those signals were not statistically secure in this dataset.
But we need to be careful. This is retrospective, single center and diagnosis code based. Temporality is uncertain. Some arrhythmic events may have occurred before or after the heart failure with preserved EF diagnosis. There was no detailed AF burden, no CMR fibrosis assessment, no ECG repolarization detail, no device level adjudication, and no medication granularity.
Association does not prove that AF causes ventricular arrhythmias. The EP Edge take is that this is not an ICD indication paper. It is a phenotype paper. AF in heart failure with preserved EF may be a marker of deeper atrial ventricular remodeling, fibrosis, autonomic imbalance, or comorbidity clustering. For now, I would use this as a reminder to take AF in heart failure with preserved EF seriously as a risk signal, not just a rate control nuisance.
The next step should be prospective work with rhythm burden, CMR, biomarkers, and adjudicated ventricular arrhythmia endpoints. Now let's move to anticoagulation after AF ablation. This is the most practiced disruptive paper in the issue but it needs careful interpretation. Current guidelines tell us to continue long term anticoagulation after AF ablation based on baseline thromboembolic risk, not on whether we think the ablation was successful, but recent randomized trials are starting to test whether that approach may be too blunt for carefully selected patients. This paper was a network meta analysis of randomized trials evaluating long term antithrombotic strategies after AF ablation.
Four randomized controlled trials were included, with three thousand nine hundred and twenty four patients. Treatment arms included oral anticoagulation continuation in nineteen sixty patients, left atrial appendage occlusion in eight zero three patients, and discontinuation of long term antithrombotic therapy or no left atrial appendage occlusion in eleven sixty one patients. The primary endpoint was ischemic stroke. Secondary endpoints included TIA and clinically relevant non major bleeding. Now the results.
The network estimate showed no significant stroke difference for oral anticoagulation versus no antithrombotic therapy. The incidence rate ratio was zero point nine zero with a ninety five percent confidence interval from 0.02 to 33.85 and a p value of 0.95. That very wide confidence interval is important. It means the estimate is imprecise because the number of events was very low. No significant stroke difference was seen for left atrial appendage occlusion versus no antithrombotic therapy either.
The incidence rate ratio was 0.79, with a very wide confidence interval from zero point zero zero to 241.01. Among patients who discontinued antithrombotic therapy without left atrial appendage occlusion, pooled stroke incidence was zero point two three events per 100 person years. Let's translate that. Events per 100 person years is a rate. If you followed 100 similar patients for one year, the estimated stroke rate would be about zero point two three events.
That is very low. In the subgroup with CHADS VASc score three or higher who discontinued therapy, pooled stroke incidence was zero point two two events per 100. A direct comparison of anticoagulation continuation versus discontinuation found no significant stroke difference, with an incidence rate ratio of 1.03 and a p value of 0.97. However, clinically relevant non major bleeding was higher with anticoagulation continuation with an incidence rate ratio of 2.49, confidence interval 1.19 to 5.23, and p value 0.02. So the signal is provocative.
But the limitations are equally important. Event counts were very low. Patients in discontinuation trials were selected. Generally younger, preserved EF, lower proportion of women, and often paroxysmal AF. Patients with prior stroke, very high CHADS VASc scores, valvular AF, and eGFR less than 30 were underrepresented or excluded.
There were no PFAERA ablation cohorts, and left atrial appendage occlusion comparisons relied heavily on sparse indirect evidence. The EP Edge take is this: This is a shared decision paper, not a guideline replacement paper. The data suggests that in selected patients with apparently successful ablation, stroke rates after stopping anticoagulation were very low. But this does not mean stop anticoagulation broadly after ablation. The safe use boundary is still narrow.
In practice, I would use a structured workflow: document ablation success, reassess AF burden, exclude high risk phenotypes that were poorly represented in the trials, discuss bleeding versus stroke trade offs, and keep reassessing risk as the patient ages or develops new comorbidities. This is becoming a serious evidence based conversation, but it is not a casual decision. The final study is a practical ECG paper. It looks at the SQRS ratio in lead I as a clue to pacemaker risk in patients with right bundle branch block. This is the kind of paper I like because it gives us a bedside measurement, not another expensive platform.
The clinical context is simple. Right bundle branch block is often treated as a right sided conduction problem, with the left bundle presumed to be normal. But that assumption is not always true. In some patients, right bundle branch block may be the visible part of broader bilateral His Purkinje disease. In lead I, the initial rapid QRS forces reflect left ventricular activation, while the terminal S wave reflects slower right ventricular activation.
The authors asked whether narrowing of the S wave could identify patients with right bundle branch block who are more likely to need a permanent pacemaker. This was a retrospective single center analysis of two eighteen patients with complete RBBB and preserved LVEF. There were one hundred and nine cases who received a permanent pacemaker for alternating bundle branch block, Mobitz II or complete heart block, or bifascicular block with abrupt, arrhythmic sounding syncope. There were also one hundred and nine controls with asymptomatic stable right bundle branch block who did not require pacemaker implantation during follow-up. The authors measured PR interval, QRS axis, QRS duration, S wave duration in lead I, and the SQRS ratio.
For patients with paired ECGs, they compared the oldest available right bundle branch block with the most recent or pre implant ECG. Here are the results. Controls were followed for about ninety months. Their QRS duration changed minimally from one hundred and forty five point two to one hundred and forty six point seven milliseconds with a p value of 0.67. Their SQRS ratio decreased slightly from 0.59 to 0.57.
Cases were followed for about eighty nine months. Their QRS duration increased from 139.9 to 147.6, with a p value less than 0.001. Their SQRS decreased from 0.52 to 0.43. Also with a p value less than 0.001, an SQRS ratio less than 0.56 was associated with need for permanent pacemaker. In the machine learning model, the odds ratio was 6.87, with a 95% confidence interval from 3.87 to 12.67 and a p value less than 0.001.
The model had sensitivity of 74.3% and specificity of seventy point six percent. Sensitivity means the test correctly identifies a reasonable proportion of patients who ultimately need a pacemaker. Specificity means it also correctly identifies a reasonable proportion who do not. The PR interval also increased among cases, from one hundred and eighty four to two nineteen milliseconds, which fits with progressive conduction disease. The limitations are important.
This was retrospective and single center. There was no invasive measurement of left bundle activation, so the mechanism is inferred rather than proven. Some control patients may have required pacemakers outside the study system later. Patients with left posterior fascicular block were excluded, so the finding may not apply to all right bundle branch block patients, and a low SQRS ratio may reflect left bundle disease, His disease, or broader conduction system disease. The surface ECG cannot separate those mechanisms by itself.
The EP Edge Take is very practical. In right bundle branch block, a short terminal S wave in lead one can mean the problem is not purely in the right bundle. An SQRS ratio less than 0.56 is not a standalone pacemaker indication, but it is a reason to look twice, especially in an older patient with syncope, PR prolongation, bifascicular disease, or progressive QRS and axis changes. Practical use: When you see right bundle branch block, do not just measure QRS width. Look at lead one.
If the S wave is less than about half of the QRS, the ECG may be telling you that the other bundle is not as healthy as it looks. Let's do a quick recap of issue 21: AI guided dispersion ablation in durable pulmonary vein isolation in ReDo AF is promising, especially when the alternative is empirical substrate modification, but it still needs randomized validation. Dual energy lattice tip ablation may improve efficiency in complex ventricular arrhythmia ablation, but the safety playbook matters as much as the efficacy signal. PFA and CIED interactions are now a real safety domain. High energy ablation near leads, coils, leadless devices, or exposed conductors requires deliberate planning and device verification.
PVC does not support routine low level tragastimulation for PVC suppression, but it teaches us a lot about sham effects, PVC variability, and neuromodulation trial design. Cannabis use is associated with increased atrial arrhythmia risk across large observational data sets so it should be part of the arrhythmia history. Postmyectomy HCM still carries residual scar mediated sudden death risk and LGE extent should remain part of ICD and follow-up discussions. AF in heart failure with preserved EF may identify a higher risk ventricular arrhythmia phenotype, but that remains hypothesis generating. Stopping anticoagulation after successful AF ablation is becoming a serious evidence based discussion, but only in carefully selected patients with continued rhythm and risk reassessment.
And finally, in right bundle branch block, a shortened terminal S wave in lead I with an SQRS ratio less than 0.56 may flag bilateral His Purkinje disease and future pacemaker risk. It is not a pacemaker indication by itself, but it should trigger closer surveillance in the right clinical setting. 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 email epedge. cast@gmail . com.
Thank you again for listening to EP Edge Journal Watch. I'm Doctor. Sharma, take care, and I'll see you till the next episode.