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Niraj Sharma: Welcome back to EP Edge Journal Watch Issue 24, June 2026. I'm Doctor. Sharma and I'm glad you are here. Before we start, thank you for the comments, questions, and suggestions. They help keep this series practical and clinically useful.
This issue is about the precision turn in electrophysiology: right patient, right target, right signal, right antithrombotic strategy, and right follow-up. We begin with persistent AF and heart failure. These patients often have atrial enlargement, fibrosis, elevated filling pressures, sleep apnea, obesity, renal disease, pulmonary hypertension, and neurohormonal activation. So AF is not just a rhythm problem, it is part of the heart failure substrate. Lee and colleagues asked a very practical first ablation question: In persistent AF with heart failure, is PVI enough, or does a broader substrate strategy improve three year outcomes?
This was a prospective multicenter randomized trial from 10 centers in China. Three hundred patients were randomized equally to one of three approaches: first, anatomic guided ablation, plus posterior wall box isolation and mitral isthmus ablation with vein of Marshall ethanol when needed second, electrogram guided ablation plus mapped driver ablation third, extensive electrogram anatomic ablation driver ablation and then anatomic ablation. The cohort included reduced, mildly reduced, and preserved ejection fraction heart failure. Follow-up used serial holters, clinic visits, monthly calls, and extra monitoring when symptoms suggested tachycardia. The co primary endpoints were cardiovascular death or heart failure hospitalization or urgent visit through thirty six months and sinus rhythm maintenance at thirty six months after a single procedure of antiarrhythmic drugs.
At thirty six months, the composite endpoint occurred in thirty six percent with anatomic guided ablation, twenty nine percent with electrogram guided ablation, and seventeen percent with the extensive strategy, p 0.01. The benefit was mainly heart failure utilization. Heart failure hospitalization or urgent heart failure visits occurred in thirty percent, twenty five percent, and twelve percent respectively, with p 0.007. Cardiovascular death was similar: six percent, four percent, and five percent. So this was not a mortality trial, it was a heart failure utilization and rhythm control trial.
Sinus rhythm maintenance also favored the extensive arm: forty four percent, fifty three percent, and sixty two percent. AF burden below one percent was achieved in fifty two percent, sixty two percent, and seventy two percent. NYHA class, six minute walk distance, and NT proBNP all improved most with the extensive strategy. Complications were low and similar. Here is the statistics translation: Compared with anatomic guided ablation, extensive ablation lowered the composite endpoint by 19 absolute percentage points from thirty six to seventeen percent.
That is an approximate number needed to treat of six over three years. Compared with electrogram guided ablation alone, the absolute reduction was 12 percentage points for an approximate number needed to treat of nine. The EP Edge Take. This is not a mandate for extensive ablation in every persistent AF patient. It is a reminder that in persistent AF with heart failure, the endpoint should not be PVI performed.
The endpoint should be meaningful AF burden reduction with a lesion set matched to atrial disease and executed durably. In practice, a patient with persistent AF, heart failure, recurrent decompensation, large left atrium, long AF duration, and advanced substrate may need more than PVI, but more ablation is only better when it is anatomically coherent, electrophysiologically justified, and technically durable. The next paper moves from atrial substrate to ventricular substrate. Redo VT ablation in non ischemic cardiomyopathy using high voltage pulsed field ablation. Redo VT in non ischemic cardiomyopathy is often not a mapping failure, it is a lesion depth failure.
The scar can be septal, mid myocardial, intramural, patchy, or epicardial. Endocardial radiofrequency may identify abnormal electrograms and still fail to reach the abnormal substrate. Kirazzo et al. Reported a single center compassionate use series from St. David's and the Texas Cardiac Arrhythmia Institute.
There were seven patients and nine procedures. Mean age was 58 years, mean LVEF was about forty percent, and all patients had an ICD or CRT defibrillator. These were redo patients with a mean of more than two prior ablations. The strategy was scar homogenization. Procedural success required non inducibility of NEVT and absence of residual abnormal electrograms in low voltage areas.
The catheter was a focal force sensing high voltage PFA catheter using a monopolar waveform greater than 10 kilovolts with QRS gated applications. Clinical VT was inducible before ablation in all patients. Acute procedural success was achieved in all procedures. Median follow-up was three twenty days. Recurrence occurred after three of nine procedures involving two of seven patients.
The safety signal was the story. There was no new conduction system disturbance, phrenic injury, or ST segment elevation, but CIED malfunction with pacing inhibition occurred in two of nine procedures and both required generator replacement. Three-dimensional mapping system malfunction occurred in three of nine procedures. Statistically, this is feasibility, not efficacy. With nine procedures, each event moves the percentage by about 11 points, so do not memorize the twenty two percent device malfunction rate as a stable estimate.
The correct interpretation is that a real electromagnetic interference signal appeared repeatedly and must be solved before routine adoption. The EP Edge Take, high voltage focal PFA may become a rescue strategy for deep intramural non ischemic VT substrate, but adoption depends on device compatibility, generator shielding, mapping system protection, interrogation protocols, backup pacing and defibrillation plans, and clear lab workflow. The lesion may be the breakthrough. Integration determines practice. Now to device EP, where the theme is sensing reserve.
An inappropriate ICD shock is not a nuisance. It can traumatize patients, trigger emergency visits, require reprogramming and sometimes lead to extraction or system conversion. The subcutaneous ICD avoids transvenous leads, which is valuable for young patients, inherited arrhythmia syndromes, limited venous access, infection risk, dialysis risk, and patients who do not need pacing, but it must interpret extrathoracic signals, so over sensing remains a vulnerability. Boyle and colleagues asked whether quantitative vector screening could reduce sensing related events compared with traditional passfail screening. The automated screening tool evaluates the primary, secondary, and alternate vectors in standing and supine positions.
Traditional screening requires at least one vector to pass in both postures, which corresponds to a quantitative score of at least 100. The authors retrieved the underlying quantitative score which incorporates QRS amplitude, QRS to noise ratio, and QT interval. QRS amplitude and signal to noise are heavily weighted, so QVS is really a sensing margin test. Starting in 2023, their protocol required one vector with standing and supine scores greater than 300 plus a second backup vector with scores greater than 100. That backup vector rule matters because it gives the clinician a reprogramming option if the first vector later fails.
Among eighty nine patients screened in the QVS era, ninety six percent would have passed traditional screening but only eighty three percent passed QVS, so QVS intentionally excluded an additional thirteen percent of candidates to avoid marginal sensing profiles. The study included two twenty three de novo subcutaneous ICD implants at the Hospital of the University of Pennsylvania, one hundred and forty five with traditional screening and seventy eight with QVS. All devices were contemporary Boston Scientific Systems, with SmartPass programmed on at implant. Follow-up was longer in the traditional group, forty two months compared with eighteen months in the QVS group, so interpretation requires caution. The primary endpoint was time to first inappropriate shock or undersensed ventricular arrhythmia.
There were twenty three events with traditional screening and two with QVS. Event rates were five point two versus one point eight per 100 patient years, with log rank p 0.02. Inappropriate shocks occurred in fifteen percent with traditional screening and three percent with QVS, an absolute reduction of about twelve percentage points. Device removal or replacement for recurrent inappropriate shocks occurred in eight percent of the traditional group and zero percent of the QVS group. SmartPass also mattered.
When SmartPass deactivated, patients became more exposed to over sensing until in person reactivation. Among 19 patients whose Smart Pass was disabled, six later had inappropriate shocks. Predictors of shorter time to inappropriate shock included younger age, history of supraventricular tachycardia, and Smart Pass deactivation. How should we read the statistics? The absolute shock reduction is clinically large but the design was not randomized.
The QVS group had shorter follow-up and practice changed over time. The trade off is explicit. QVS reduces inappropriate shocks, but it reduces subcutaneous ICD eligibility. The EP Edge take moved from a door test to a reserve test. The old question was, Does the patient pass screening?
The better question is Does this patient have one strong vector and one backup vector to live safely with an extravascular sensing system for years? If sensing reserve is poor, consider an extravascular ICD or transvenous ICD rather than forcing a subcutaneous system. From device sensing, we move to patient generated sensing. Wearables are already in EP clinics and cardiology inboxes. The European Heart Journal review by Hughes et al.
Covered wearable sensors, regulation AF screening, heart failure monitoring, cuff less blood pressure activity and sleep metrics, clinical trials, artificial intelligence and EHR workflow. The first practical point: a smartwatch ECG, a cardio strip, a PPG alert, a chest patch, and a consumer sleep score are not the same clinical instrument. ECG based tracings are most useful for EP because they can confirm rhythm during symptoms or alerts. PPG can screen for irregular pulse patterns, but it is not ECG confirmed AF. Motion artifact, ectopy, sinus arrhythmia, and poor signal can create false positives.
Activity sensors may matter as functional endpoints. Step count and activity trends can help in heart failure, frailty, rehab, and post procedure recovery. Cuffless blood pressure is promising, but calibration, posture, temperature, vascular tone, and user factors mean it should not replace validated cuff measurement. The AF screening studies illustrate why statistics need context. In the Apple Heart Study, more than four hundred and nineteen thousand adults were enrolled and only zero point five two percent received an irregular pulse notification.
Among those who returned confirmatory patches, positive predictive value was eighty four percent. In the Fitbit Heart Study, more than 455,000 adults were enrolled, about one percent received a notification, and positive predictive value in the confirmatory workflow was ninety eight percent. But positive predictive value depends on prevalence, signal quality, algorithm, and confirmatory workflow. It does not automatically mean population screening reduces stroke. Amalfi made that point: Patch screening modestly increased AF diagnosis in older adults with stroke risk, with a ratio of proportions of 1.26 and p 0.03, but stroke was not reduced.
Detection is not the same as outcome improvement. Wearables may also help with heart failure surveillance and rate control assessment. In Link HF, a multisensor chest patch in one hundred recently hospitalized heart failure patients predicted readmission with eighty five percent specificity and seventy six-eighty eight percent sensitivity, with alerts a median of six point five days before readmission. The signal may precede the hospitalization, but the health system still has to act fast enough to change the outcome. Chief H.
F. Used Fitbit Versa in a remote heart failure trial, daily step count correlated with Kansas City Cardiomyopathy Questionnaire scores suggesting that real world activity can become a patient centered endpoint. Rate AF used Fitbit Charge in permanent AF with heart failure and showed wearables can help evaluate rate control at rest and with exertion. The bottleneck is workflow. Wearable data often sit in vendor apps rather than structured EHR fields.
The data can be too large, poorly labeled, hard to validate, and not assigned to a responsible reviewer. Without triage rules, wearables create anxiety, documentation burden, and unnecessary testing. A practical EP wearable policy should separate four groups: actionable ECG documentation, screening alerts that need confirmation, longitudinal trends such as declining steps or rising resting heart rate, and non validated consumer scores that should not drive major decisions. The EP Edge take: Wearables are useful when they answer a clinical question. A symptomatic ECG strip showing AF is useful.
A PPG alert that leads to confirmatory monitoring may be useful. A step count decline in a heart failure patient may be useful. But raw data without thresholds, responsibility, documentation, and escalation rules is not medicine. The next frontier is not more sensors it is governed interpretation. Next is Opinion.
The surgical left atrial appendage occlusion trial in valvular heart disease without known AF. This trial asked a common surgical question: If a patient is undergoing valve surgery, has no known AF or atrial flutter, but has an elevated CHADS VASc score and a high future risk of postoperative AF, should the appendage be closed prophylactically? Opinion was a multicenter, open label, randomized, superiority trial at three Chinese cardiac surgery centers. It included two thousand one hundred and eighteen patients, ten sixty two assigned to surgical appendage occlusion, and ten fifty six assigned to no appendage intervention. Patients were undergoing mitral or aortic valve repair or replacement, had no baseline AF or flutter, and had a CHADS VASc score of at least two.
The appendage was amputated and closed with a two layer suture with intraoperative TEE confirmation. The primary endpoint was ischemic stroke or cardiovascular mortality at one year. The primary endpoint occurred in six point nine percent, with appendage occlusion and eight point two percent in controls. The hazard ratio was 0.83, with a 95% confidence interval from 0.61 to 1.14 and p 0.25. The hazard ratio suggests a possible 17% relative reduction, but the confidence interval crosses one.
This is statistically neutral. The absolute difference was only 1.3 points at one year. Ischemic stroke was identical at two point five percent in both groups, and postoperative AF was also not significantly different. The EP Edge take: Opinion should slow routine prophylactic appendage closure in non AF valve surgery patients, but it does not permanently close the question. Known AF during cardiac surgery is one phenotype.
No known AF, valve surgery, postoperative anticoagulation, perioperative inflammation, and uncertain future AF is another. In practice, do not confuse future AF risk with established appendage mediated thrombotic disease. The appendage matters most when the appendage is the mechanism. The next paper is the European Society of Cardiology and European Association for Cardiothoracic Surgery Consensus Statement on Antithrombotic Therapy after Coronary Artery Bypass Surgery. This is directly relevant to EP because bypass patients often develop postoperative AF, already have established AF, or need both antiplatelet therapy and oral anticoagulation.
The clinical balance is graft patency, ACS indication, bleeding risk, surgical healing, renal function, frailty, postoperative AF, and established AF. For chronic coronary syndromes, low dose aspirin should generally be continued perioperatively and restarted within twenty four hours after surgery, ideally within six hours. Long term aspirin remains foundational. For selected low bleeding risk patients with high graft failure risk, DAP for twelve months may reduce graft failure. For ACS patients after bypass, DAP for twelve months remains standard when bleeding risk is controlled.
The graft patency data are real but come with bleeding cost. Compared with aspirin alone, ticagrelor dAPT reduced saphenous vein graft failure with an odds ratio around zero point five and number needed to treat around ten. Clopidogrel dAPT also reduced graft failure with an odds ratio around zero point six and number needed to treat around nineteen, but ticagrelor DAPT increased clinically important bleeding, with an odds ratio close to three. For EP, the key distinction is postoperative AF versus established nonvalvular AF. Postoperative AF occurs in roughly twenty to thirty percent of bypass patients and is associated with recurrence, stroke risk, and healthcare utilization, but it can also reflect transient surgical inflammation, atrial stretch, volume shifts, pericardial irritation, electrolyte disturbance, and autonomic imbalance.
So a single brief postoperative AF episode should not automatically be treated like chronic nonvalvular AF. The evidence for anticoagulation in postoperative AF is mixed. One large observational study suggested early oral anticoagulation was associated with lower stroke risk, with an adjusted hazard ratio of zero point five five, but other studies showed no clear thrombotic reduction and more bleeding or mortality. A meta analysis of 28 observational studies, including more than 1,600,000 bypass patients, found no significant thromboembolic reduction with oral anticoagulation and higher bleeding risk. So postoperative AF matters, but routine anticoagulation for every episode is not supported.
Burden matters. A small loop recorder study showed recurrent AF after bypass, but median AF burden beyond the first postoperative month was only 0.1. Duration, recurrence, symptoms, hemodynamic effect, discharge rhythm, and stroke risk all matter. The consensus is clearest when AF persists at discharge. Start oral anticoagulation when bleeding risk allows, and reassess after four weeks.
If the patient is back in sinus rhythm at discharge, four weeks of anticoagulation may be considered depending on AF burden, bleeding risk, thromboembolic risk, and likelihood of recurrence. For established non valvular AF before bypass, restart oral anticoagulation when surgically safe. Doex may be restarted around two to three days after bypass if bleeding risk is acceptable. Vitamin K anticoagulant patients may need heparin bridging until the INR is therapeutic. Avoid routine triple therapy.
If oral anticoagulation is required after bypass, the default should usually be oral anticoagulation plus a single antiplatelet agent, not oral anticoagulation plus aspirin plus a P2Y12 inhibitor. After twelve months, many patients can transition to oral anticoagulation alone. The EP Edge take: Do not ignore postoperative AF, but do not create lifelong anticoagulation by inertia, define burden, estimate stroke and bleeding risk, avoid triple therapy, use oral anticoagulation plus single antiplatelet therapy when needed, reassess at four weeks, and monitor rhythm after discharge. Finally, the off track paper: Genetic predictors of GLP-one receptor agonist weight loss and side effects. This is not an EP trial, but it matters because obesity, diabetes, sleep apnea, HFpEF, left atrial enlargement, epicardial adiposity, AF progression, ablation recurrence, procedural risk, and long term substrate progression are now part of the same cardiometabolic substrate.
The question was whether common genetic variants help explain why some patients lose substantial weight on tirzepatide while others lose less or stop because of nausea or vomiting. This was a 23andMe genome wide association study of twenty seven thousand eight hundred and eighty five self reported GLP-one medication users. Participants were mostly female, median age 52 years, predominantly European ancestry, with median baseline BMI about thirty five and median therapy duration about eight months. The primary efficacy phenotype was percentage BMI change. Side effect phenotypes focused on moderate to severe nausea and vomiting.
Replication for weight loss used the All of Us cohort. A missense variant in GLP-1R was associated with greater weight loss (about 0.76 kilograms per effect allele). GLP-1R variants were also associated with nausea and vomiting, and a GIPR signal was identified for vomiting among GLP-one treated participants. Combined genetic and non genetic models explained about twenty five percent of BMI loss variants, but side effect prediction was modest, with AUC values around 0.65 to 0.68. The EP Edge Off Track Take This is future shaping, not practice changing.
The counseling message is that response variability and GI intolerance are partly biological, not simply adherence or willpower. For EP, this is substrate prevention. The atrium does not begin remodeling in the EP lab. Let's close with a quick recap. Persistent AF with heart failure emphasized substrate match burden reduction.
Redo non ischemic VT highlighted deep lesion promise with major integration issues. Subcutaneous ICD screening moved from passfail to sensing reserve. Wearables require confirmation and governed workflow. Opinion slowed routine prophylactic appendage closure in non AF valve surgery Post bypass AF management requires burden assessment, bleeding risk awareness and four week reassessment and GLP-one and GIP pharmacogenomics points toward cardiometabolic substrate prevention. All references and graphics are available on the LinkedIn newsletter, EP Edge Journal Watch, as well as on Substack, epedge.
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Take care and bye for now.