Niraj Sharma: Welcome back to EP Edge Journal Watch. I am Doctor Sharma. Thanks for spending a few minutes with me at the cutting edge of electrophysiology decision making. This is Issue 14 March 2026 Ablation at the Extremes Octogenarians Heart Failure and Left Atrial Appendage Paradox plus Renal Safety Signals and Timing. Quick Roadmap Rehealth AF in patients age 80 and above Polar heart failure On pulmonary vein isolation only in heart failure Option in OCEAN Multi morbidity and long term recurrence after cryo balloon ablation hemolysis and acute kidney injury after pulsed field ablation, timing of repeat ablation, the Paced score for ejection fraction recovery post AF ablation, left bundle branch area pacing upgrades for pacing, induced cardiomyopathy, and a bonus trial on left ventricular thrombus prevention after anterior myocardial infarction.
Let's start with the very elderly. Study one Re Health AF, a prospective multicenter registry from 47 Japanese centers, seven zero three atrial fibrillation patients age 80 or older, ablation in two forty nine, versus conservative management in four fifty four. Methodology. Primary endpoint: a composite of thromboembolic events, other cardiovascular events, bleeding, and all cause death. They used propensity score matching with 193 match pairs plus sensitivity analyses.
Importantly they also tracked one year patient centered outcomes results. On hard outcomes, the study was directionally favorable but not definitive: nine point six percent versus twelve point four percent overall, hazard ratio 0.78, and 7.3 versus 10.9 in the matched cohort, hazard ratio 0.65, both statistically non significant with inconsistent signals across adjusted models. Where the signal was consistent was function. Compared with conservative care, ablation was associated with larger symptom improvement, about a 10 quality of life gain, more favorable changes in nutrition and cognition, and reductions in NT proBNP and left atrial size. Recurrence after ablation was about twelve percent and recurrence tracked with higher risk.
Critical appraisal. The limitations are the ones you expect: non randomized selection, a heterogeneous composite, and follow-up that may be too short to see clean separation on hard endpoints in a competing risk population. But it is a strong reminder that in octogenarians what matters most may be symptoms, independence, and cognitive trajectory. EP edge take. In very elderly patients, the value proposition of ablation is quality adjusted time.
Start with goals and symptom burden, then calibrate expectations using substrate markers. Persistent atrial fibrillation, left atrial size, and frailty. Advanced age alone is not the contraindication. Poor substrate and limited reserve are. Now let's move to heart failure, where the ablation conversation is often framed as a binary versus more lesions for more substrate.
The problem is that in heart failure time, fluid shifts and procedural complexity are not academic details. They can change the entire risk benefit equation. Study two. Polar heart failure. This asks a clean operational question.
If we commit to a standardized cryoballoon pulmonary vein isolation only strategy, can we achieve rhythm outcomes in heart failure with reduced ejection fraction that are non inferior to patients without heart failure? Prospective observational single center designed as a non inferiority analysis. Consecutive first time cryoballoon pulmonary vein isolation for paroxysmal or persistent atrial fibrillation. Heart failure with reduced ejection fraction was defined as a left ventricular ejection fraction 40% or less with heart failure symptoms. They then used propensity matching one to five, leaving a matched cohort of one hundred and seventy four heart failure patients compared with eight seventy non heart failure patients with about two years of follow-up.
The primary efficacy endpoint was simple and familiar. The first documented recurrence of atrial fibrillation, atrial flutter, or atrial tachycardia after a ninety day blanking period. So this is time to first recurrence, not continuous burden, and that matters when we interpret it. The recurrence endpoint was essentially identical: forty three point seven percent in heart failure, forty three point six percent in non heart failure, meeting non inferiority. Mortality was numerically higher in heart failure (6.3 versus three point four percent and procedure related adverse events were low and similar (roughly three-four percent ).
Critical appraisal: This is not a prognosis trial. It is not measuring heart failure, hospitalization or survival. It also lacks continuous rhythm monitoring, which means it can miss asymptomatic recurrence and it cannot quantify atrial fibrillation burden, but it does something valuable. It supports a reproducible, lower complexity pulmonary vein, isolation only default strategy in heart failure, at least for rhythm recurrence outcomes, when you are trying to avoid adding procedural time and risk without proven incremental yield. EP edge take.
Here is how I translate polar heart failure into practice: one. In heart failure, your first job is durable pulmonary vein isolation. If you cannot do that reproducibly and safely, adding more lesions is not advanced. It is uncontrolled complexity. Two.
Do not confuse non inferior recurrence with equivalent clinical benefit. In heart failure, what we truly want is burden reduction, improved ventricular function, fewer admissions, and better symptoms. A pulmonary vein isolation only strategy can be a defensible start, but outcomes will hinge on what you do next: objective rhythm surveillance, early identification of clinically meaningful recurrence, and a disciplined approach to repeat strategy. Three. Patient selection is everything.
The patients most likely to fail a pulmonary vein only strategy are the ones with advanced atrial myopathy, large atria, long standing persistent atrial fibrillation, heavy fibrosis signals, or recurrent organized atrial tachycardias. In those patients, pulmonary veins only may be step one, not the entire plan. Operationally I would build a heart failure ablation pathway around three checkpoints. Checkpoint one: Pre procedure substrate and goals. Checkpoint two: Early post ablation monitoring focused on burden and symptoms.
And checkpoint three: a rapid decision window if recurrence is meaningful, because waiting for months of drift is how substrate progresses and yield declines. Next is our left atrial appendage cluster, because the appendage has become the most common second procedure conversation after ablation. Patients often ask a deceptively simple question: If I close the appendage, does that help my rhythm? And if I don't have recurrence, can I stop anticoagulation? These studies help separate those ideas.
Study three: Option trial sub analysis: Atrial fibrillation recurrence after left atrial appendage closure methodology. This is a rhythm focused sub analysis within a larger randomized trial of post ablation patients. About sixteen hundred patients were randomized to left atrial appendage closure versus continued anticoagulation after atrial fibrillation ablation. In the closure arm, roughly forty percent were done concomitantly and sixty percent were staged. Rhythm recurrence was followed through thirty six months, assessed by device interrogation when an implanted device existed and by 12 lead electrocardiograms in those without devices.
At thirty six months, atrial fibrillation recurrence was forty nine point two percent with appendage closure versus forty five point five percent without closure, not statistically different. Concomitant versus stage closure looked the same, and stroke or systemic embolism rates were low and similar, irrespective of recurrent status, (about one to one point three percent ). Critical appraisal: rhythm ascertainment was not continuous for most patients, which means time to first recurrence underestimates total burden, and rhythm was not the primary objective of the overall trial, So this sub analysis is not built to detect small rhythm differences, but the main signal is clinically stable. Appendage closure appears largely rhythm neutral in a modern ablation population. EP edge take.
Here is the key behavioral correction. Do not confuse mechanical closure with electrical isolation. Appendage closure is a stroke and bleeding strategy decision, not a rhythm strategy decision. If you are closing the appendage to help ablation work, you are targeting the wrong mechanism. Second, do not let no recurrence seduce you into thinking stroke risk is gone.
Risk is not simply an electrocardiogram state, it's vascular biology, atrial disease and comorbidity. Even in this dataset, stroke and systemic embolism remained low and did not materially depend on whether recurrence was documented. Another reminder that absence of detected recurrence is not absence of risk. Third, if you do a combined procedure anticipate early noise, inflammation, volume shifts, transient triggers and judge success by burden and clinical trajectory, not by a single early episode. That means you should decide ahead of time what your monitoring tool is implantable device, wearables, patch monitoring and what burden threshold triggers action.
Study four. Ocean left atrial appendage closure, spontaneous echo contrast and outcomes after appendage closure. Methodology. Registry of twelve seventy six patients undergoing appendage closure with WATCHMAN two point five or WATCHMAN FLEX. Pre procedure transesophageal echo.
Spontaneous echo contrast was graded. None, mild to moderate and severe. Severe spontaneous echo contrast was about thirteen percent of the cohort. Outcomes were thromboembolic events, device related thrombus, and major bleeding. Severe spontaneous echo contrast had higher event rates, thromboembolic events eleven point five percent in severe versus four point four percent with none, and device related thrombus increased stepwise, about two point eight percent with none, eight point four percent with mild to moderate, and twelve point four percent with severe.
After adjustment, spontaneous echo contrast grade alone was not independently predictive of thromboembolism, but the combination of severe spontaneous echo contrast plus non paroxysmal atrial fibrillation was strongly predictive, adjusted hazard ratio about two point five for thromboembolism and nearly three for device related thrombus. EP edge take: This is the most actionable message of the entire appendage cluster. Treat severe spontaneous echo contrast as a substrate marker not a procedural nuisance. It is a bedside sign that atrial disease biology, stasis, endothelial dysfunction, hypercoagulability remains active after closure. So operationally if I see severe spontaneous echo contrast especially with non paroxysmal atrial fibrillation, I change two things: one.
I intensify post device imaging surveillance. I do not treat the forty five day check as a formality. I am looking actively for device related thrombus and leak and I have a low threshold for additional imaging if symptoms or device parameters change. Two. I become deliberate about antithrombotic strategy.
For carefully selected high risk patients, extended anticoagulation or reduced dose anticoagulation can be reasonable rather than a reflex device equals stop anticoagulation. The decision is individualized but the principle is universal. Severe spontaneous echo contrast is a warning that the patient's biology wants to thrombose. In other words, appendage closure is not an eraser. It is a mechanical intervention layered on top of an atrial disease state.
OCEAN appendage closure tells you which patients remain biologically high risk even after you've solved the appendage. Now let's address the uncomfortable reality of modern atrial fibrillation practice. Most patients are not single disease atrial fibrillation, they are multi morbidity patients and the atrium behaves differently when the body is metabolically inflamed, hypertensive, obese, sleep deprived, diabetic, and heart failure prone. Study five: Questioning the role of pulmonary vein isolation in multi morbid patients. Prospective single center cohort of fourteen oh two patients undergoing first time cryoballoon pulmonary vein isolation for paroxysmal or persistent atrial fibrillation.
Comorbidity burden was stratified using a CHADSWAS score. Four or more was high burden (about three thirty two patients) versus low burden (in about ten seventy). They tracked atrial arrhythmia recurrence after blanking, out to five years, and also evaluated short term safety and longer term serious adverse events. At one year, recurrence was numerically higher in the high burden group (26.4 versus twenty two point one percent ) but not statistically significant. By five years the curves separated meaningfully: sixty four point four percent recurrence with high burden versus fifty three point one percent with lower burden.
Thirty day safety was similar but overall serious adverse events were higher in high burden patients, largely driven by mortality. In multi variable analysis, age 75 or older emerged as the only independent predictor of recurrence, Critical appraisal, this is non randomized and comorbidity burden likely correlates with unmeasured atrial myopathy and fibrosis. Rhythm monitoring intensity can also bias recurrence estimates, especially because asymptomatic recurrence is more common than we admit. Still, the long term separation is hard to ignore. EP edge take.
This paper forces a reframing. In multi morbid atrial fibrillation, are we optimizing the right outcome? If the dominant five year risk is driven by non arrhythmic substrate and mortality, then a rhythm recurrence curve is not the only or even the primary success metric. Here is how I apply this clinically: one. I still offer pulmonary vein isolation to multi morbid patients when symptoms or atrial fibrillation burden justify it, but I reset the goal from durable sinus rhythm forever to symptom relief plus burden reduction.
That expectation management changes patient satisfaction and reduces the sense of failure when recurrence happens. Two. I treat ablation as one component of a comprehensive atrial disease program. If the comorbidity stack is untreated then ablation becomes a mechanical solution to a biologic problem and biology wins over years. Three.
I lower the threshold for early recurrence management. That does not mean redo everyone. It means you do not ignore recurrence for twelve months while the atrium remodels. Three. Is this pulmonary vein reconnection, triggers, or progressive substrate?
Then you decide rapidly whether the next step is medication optimization, cardioversion strategy, or a targeted redo. Bottom line: In high comorbidity burden patients, pulmonary vein isolation may still be appropriate, but the highest value care often comes from what surrounds the ablation: upstream therapy, realistic monitoring, and timely response to recurrence. Now two very practical papers, because they change what you do in the lab and what you do the day after the lab. First pulsed field ablation and renal safety signals. Second when to redo an ablation after recurrence.
Study six: acute kidney injury and haptoglobin depletion after pulsed field ablation, impact of device type under routine hydration. Single center retrospective cohort of two eleven consecutive atrial fibrillation patients undergoing an initial pulsed field ablation between October 2024 and March 2025. Two systems were compared: Farapulse in 01/2017 and PulsaSelect in '94. They used a routine hydration protocol of fifteen hundred milliliters of intravenous saline. Severe hemolysis was defined as haptoglobin depletion below the assay's lower detection limit.
Acute kidney injury was defined by KDIGO criteria (a creatinine rise of at least 0.3 mgdL within forty eight hours). Haptoglobin depletion was common (twenty seven percent overall) and higher with Ferrapulse than Pulse Select (thirty seven versus fourteen percent ). Acute kidney injury was uncommon six percent overall and similar by device about seven versus five percent. Predictors of acute kidney injury were higher body mass index and lower baseline estimated glomerular filtration rate. Importantly, acute kidney injury was not clearly associated with haptoglobin depletion or device type in multivariable models.
Critical appraisal: low event counts limit multivariable stability. And biomarkers were measured only the next day, which can miss later or transient changes. Still, this is enough signal to justify protocolization. EP edge take. This is a workflow paper disguised as a safety paper.
Two pragmatic actions for twenty twenty six Pulsed Field Practice. Action one: Risk stratify renal vulnerability before the case. Baseline eGFR and body habitus matter more than the marketing name of the catheter. If eGFR is limited or BMI is high, treat the case as a renal risk case. Optimize hydration strategy, avoid nephrotoxins and plan post procedure lab checks.
Action two: Build a post PFA lab and symptom bundle. For higher risk patients a next day creatinine is reasonable. Consider adding hemolysis markers when clinical suspicion exists, especially if urine is dark or the patient has flank discomfort. The goal is not to over test, it is to detect the small subset of patients who will convert a benign hemolysis signal into a meaningful renal injury and prolonged stay. And one more nuance: do not over interpret device differences in hemolysis without translating into clinical harm.
The clinically meaningful endpoint here is acute kidney injury and prolonged care, and those concentrated in the predictable phenotype high BMI and low baseline EGFR. Study seven. Repeat ablation timing for recurrent atrial fibrillation. Prospective multicenter cohort of eleven forty four patients with recurrent atrial fibrillation undergoing repeat ablation at three hospitals. They stratified the recurrence to repeat ablation time into quartiles zero to twelve months, thirteen-thirty three, thirty four-fifty six, and fifty seven months or more.
Monitoring was scheduled Holters at three, six, nine, and twelve months plus symptom driven evaluation. The primary endpoint was freedom from atrial fibrillation or atrial tachyarrhythmia recurrence longer than thirty seconds off antiarrhythmic drugs at twelve months after blanking. Earlier redo correlated with better outcomes. Seventy one percent freedom from recurrence in the zero to twelve month group versus about sixty two percent in the middle quartals and fifty five percent in those waiting nearly five years or more. Shorter DART also tracked with better quality of life improvement and lower longest atrial fibrillation episode measures at follow-up.
This does not mean redo everyone early. It means do not let redo decisions drift. The longer you wait with meaningful recurrence, the more time you give the atrium to progress, and the lower the procedural yield becomes. So the practice changes a decision framework. Once recurrence is documented and clinically meaningful, you perform an early phenotype assessment, pulmonary vein reconnection, triggers or progressive substrate, and then you choose a path quickly.
If the plan is a redo, aim within about twelve months when feasible. If the plan is medical therapy, fine, but make it intentional and time limited with a reassessment point. In other words, treat recurrence as a fork in the road, not as a background symptom that you tolerate for years. Next, two studies that are highly useful at the bedside, because they give you predictive structure. First, who recovers ejection fraction after atrial fibrillation ablation?
Second, how reliably left bundle branch area pacing reverses pacing induced cardiomyopathy. Study eight, left ventricular ejection fraction response after atrial fibrillation ablation, the PACE score, methodology, multicenter cohort of three sixty six patients with atrial fibrillation, and left ventricular ejection fraction under fifty percent undergoing an index ablation. A responder was defined as either an absolute ejection fraction increase of at least 10% or improvement to 50% or more on follow-up echo after the final ablation. Predictors were derived via multivariable logistic regression stratified by rhythm status at follow-up. About seventy one percent were responders, in the subgroup that was in sinus rhythm at follow-up.
Predictors of non response were heart failure etiology, QRS duration greater than one hundred and five milliseconds, paroxysmal atrial fibrillation, and type two diabetes forming the Paste score. Discrimination was strong, with a C statistic around 0.83. A score under two predicted a high probability of response (about eighty seven percent ), while a score three or more enriched for non response, and in a cardiac MRI sub cohort, late gadolinium enhancement was much more common among non responders. EPH take. PACE is valuable because it converts a vague promise your ejection fraction might improve into a quantified counseling tool.
But here is the deeper lesson: when ventricular dysfunction is scar driven, rhythm control alone cannot fully reverse the phenotype. That late gadolinium enhancement signal is the biology statement behind the score. Practically I use PACE in three ways: one. To set expectations and avoid over promising. Two.
To decide how aggressively to pursue objective rhythm surveillance, because responders are often the patients who truly achieved meaningful burden reduction. Three. To trigger early heart failure device planning when non response probability is high. That means early collaboration about CRT or conduction system pacing and not waiting for months of persistent low EF before acting. And an important caution, do not use paste as a gatekeeper to deny ablation.
Use it to build the plan around the ablation, Monitoring, escalation pathway, and device strategy when needed. Study nine. Outcomes of left bundle branch area pacing upgrade in right ventricular pacing induced cardiomyopathy. Methodology. Observational retrospective multicenter study of sixty four patients with pacing induced cardiomyopathy upgraded to left bundle branch area pacing.
Baseline ejection fraction averaged about 36%, New York Heart Association class about 2.7 and paced QRS duration about 172. They tracked electrical and echocardiographic response and longer term device performance. Upgrade success was high with QRS narrowing from about one hundred and seventy two to one hundred and thirty three milliseconds. Mean ejection fraction improved by about 11% and functional class improved meaningfully. Lead extraction was performed in about twenty eight percent, nearly one in three, and yet over roughly twenty seven months of follow-up, there were no long term complications and no need for lead revision.
Outcomes were similar regardless of whether right ventricular pacing burden was above or below 90%. EP Edge Take. The clinical message is simple: pacing induced cardiomyopathy is often reversible, and LBP pacing is an operationally strong way to deliver physiologic resynchronization, predictable QRS narrowing, meaningful EF improvement, and a low long term revision burden. The operational message is what I care about. Extraction strategy is not rare.
Nearly one in three needed extraction, so an upgrade program needs a deliberate pathway: imaging, venous access planning, extraction readiness, and follow-up rhythm and EF monitoring. So my take home algorithm is suspect pacing induced cardiomyopathy early, confirm with pacing burden and timeline, and upgrade before advanced remodeling. When you act early, the probability of reverse remodeling is higher and the patient avoids months of avoidable heart failure exposure. Finally, a cardiology bonus that intersects with electrophysiology because we live in the world of competing thrombotic and bleeding risk, especially in patients who end up on multiple antithrombotic agents. Study 10, a peritif low dose rivaroxaban to prevent left ventricular thrombus after anterior myocardial infarction.
Multi center open label randomized trial with blinded endpoint assessment across 29 centers in France, nested within a registry. Five sixty anterior ST elevation myocardial infarction patients were randomized to dual antiplatelet therapy plus rivaroxaban 2.5mg twice daily for four weeks versus dual antiplatelet therapy alone. The primary endpoint was left ventricular thrombus detected by contrast enhanced cardiac MRI at one month. The trial was negative. Left ventricular thrombus occurred in thirteen point seven percent with rivaroxaban versus sixteen point six percent with dual antiplatelet therapy alone, numerically lower but not statistically significant.
Major bleeding was similar, but minor bleeding was clearly higher with rivaroxaban, about sixteen percent versus seven percent. Critical appraisal: a negative endpoint with limited power cannot exclude a modest benefit and the four week duration may miss later thrombus dynamics. But the direction is clear: in an unselected anterior ST elevation MI population, the thrombus signal is not strong enough to justify routine triple therapy, especially when nuisance bleeding rises substantially. EP edge take: Do not routinize prophylactic low dose rivaroxaban on top of dual antiplatelet therapy solely to prevent left ventricular thrombus, at least with this dose, duration and imaging define endpoint. If you consider adding anticoagulation, it should be for a clearly defined high risk phenotype, a large akinetic apex, severe systolic dysfunction or early imaging suggesting thrombus formation risk, and even then, you should choose the shortest effective duration and reassess with imaging rather than leaving triple therapy on autopilot.
EPH bottom line. Issue 14. In octogenarians, ablation may not reliably move heart outcomes short term, but it can improve symptoms, quality of life, and functional health markers, making shared decision making the core endpoint. In heart failure with reduced ejection fraction, a standardized cryoballoon, pulmonary vein isolation only strategy can deliver non inferior rhythm outcomes versus non heart failure cohorts, supporting simplicity first when durable pulmonary vein isolation is the goal. Left atrial appendage closure appears rhythm neutral after ablation.
Choose it for stroke and bleeding strategy, not rhythm benefit. Severe spontaneous echo contrast, especially with persistent atrial fibrillation, identifies a high risk biology phenotype, intensifies surveillance, and be deliberate about post closure anticoagulation strategy. Comorbidity burden predicts worse long term recurrence after pulmonary vein isolation. Reset expectations towards symptom and burden control and invest heavily in upstream therapy. Pulsed field ablation associated hemolysis signals are common.
Clinically significant acute kidney injury is uncommon, under routine hydration but concentrates in higher BMI and lower eGFR patients. Protocolize hydration and monitoring. Earlier repeat ablation within about twelve months of recurrence diagnosis is associated with better rhythm and quality of life outcomes when a redo strategy is chosen. Paste provides a pragmatic way to counsel patients with left ventricular dysfunction on recovery likelihood after ablation, with scar biology as the dominant non response signal. Left bundle branch area pacing upgrade is a viable resynchronization strategy for pacing induced cardiomyopathy with meaningful electrical narrowing and reverse remodeling.
Thank you for listening to EP Edge Journal Watch. All graphic details and references will be available on epedge.substack.com as well as on the LinkedIn newsletter EP Edge Journal Watch. If you have questions or suggestions email me at epedgecastgmail. com. Until next time take care.