Pulsed field ablation works on the principle of irreversible electroporation: extremely short, high-voltage electric pulses punch nanoscale pores into cell membranes, killing cardiomyocytes while largely sparing neighboring structures. Because different tissue types have different thresholds for irreversible injury, PFA is inherently tissue-selective. That selectivity is what has made it so attractive compared with thermal techniques such as radiofrequency and cryoablation, which can inadvertently damage the esophagus, the phrenic nerve, or the coronary arteries that lie close to the pulmonary veins—the trigger sites for most paroxysmal atrial fibrillation.

Early PFA platforms relied on monophasic pulses, which are simple to generate and highly efficient at electroporating cells, but they came with a well-documented set of problems. Monophasic stimulation provoked violent skeletal muscle contractions, required deep anesthesia, and drove unwanted electrochemical reactions at the electrodes, including polarization and gas formation. Biphasic waveforms—pairs of pulses with opposite polarity—were introduced to balance the delivered electrical charge, dramatically reducing muscle stimulation and electrochemical byproducts. Today, essentially every major commercial platform, from FARAPULSE to VARIPULSE to PulseSelect, uses some form of biphasic delivery.

But symmetric biphasic designs carry their own subtle biophysical trade-offs. When the second, opposite-polarity phase immediately follows the first, it can partially cancel the transmembrane potential that the first phase built up—a phenomenon known as the charge-cancellation effect. Compensating for that inefficiency requires higher electric field strengths, and pushing more energy through dense, high-frequency pulse bursts can generate unintended Joule heating, microbubble formation, and acute hemolysis. Those complications are not theoretical: silent cerebral lesions and hemolysis-related kidney injury have both emerged as safety concerns in the broader PFA literature.

The Chinese team, led by researchers at Tianjin Medical University and collaborating hospitals, took a different route. Their system delivers each pulse as an asymmetric biphasic waveform—a 7-microsecond positive phase followed by a 3-microsecond negative phase, separated by a 5-microsecond interval—at an amplitude of 1,000 volts. The catheter itself is a 10.5 French device with six adjustable splines, each carrying a single electrode. During each pulse, three electrodes act as anodes and three as cathodes. The catheter can be partially expanded into a basket shape to advance into a pulmonary vein, then fully deployed into a flower configuration with a maximum diameter of 32 millimeters at the vein’s ostium, maximizing tissue contact for ablation.

The trial, registered as ChiCTR2200062157, enrolled patients between January 2022 and December 2024. All had symptomatic paroxysmal atrial fibrillation that had failed or could not be tolerated on at least one class I or class III antiarrhythmic drug. Fifteen patients withdrew before the procedure, leaving 105 who underwent ablation and completed the prespecified 12-month follow-up. The cohort had a mean age of 63.7 years, was 60 percent male, and carried a mean CHA2DS2-VASc stroke-risk score of 1.54. Procedures were performed under general anesthesia or conscious sedation with uninterrupted oral anticoagulation and heparin to maintain an activated clotting time of at least 300 seconds.

The procedural results were striking. All 420 targeted pulmonary veins were acutely isolated—a 100 percent acute success rate—and no vein reconnected during the mandatory 20-minute waiting period after ablation. The mean ablation time, from the first PFA application to the last, was just under 219 seconds, and the mean total procedure time was about 102 minutes. Post-ablation voltage mapping, performed in roughly half the patients at the operator’s discretion, confirmed complete isolation at the pulmonary vein antra with no evidence of unintentional lesion formation elsewhere in the left atrium.

At 12 months, the Kaplan–Meier estimate of freedom from atrial arrhythmia recurrence—atrial fibrillation, flutter, or tachycardia lasting at least 30 seconds on protocol-specified monitoring—was 69.5 percent, with a 95 percent confidence interval of 60.1 to 77.5 percent. That figure sits comfortably within the range reported for other PFA technologies. The SINGLE SHOT CHAMPION trial reported 62.9 percent one-year freedom from recurrence, the PULSED AF Pivotal Trial reported 66.2 percent, and the VOLT-AF IDE study reported 81.1 percent. Importantly, no patient in the Chinese trial underwent repeat ablation during the 90-day blanking period, whereas several comparator studies permitted repeat procedures without counting them as endpoint failures—a difference the authors flag when urging caution about direct cross-study comparisons.

On the safety front, the results were equally notable. Not a single case of pulmonary vein stenosis, phrenic nerve injury, atrioesophageal fistula, stroke, cardiac tamponade, or acute kidney injury was recorded across the entire 12-month follow-up. The primary safety endpoint—a predefined serious adverse event—occurred in just one patient (0.95 percent), who experienced a transient coronary vasospasm on postoperative day three that resolved completely after intracoronary vasodilator administration. That patient had a pre-existing high-grade atherosclerotic coronary lesion, and while the authors acknowledge that a contributory role of the PFA procedure cannot be entirely excluded, the episode underscores a known pattern: ST-segment elevation during or after PFA should prompt urgent coronary angiography and nitroglycerin, and prophylactic nitrates may be worth considering when ablating near coronary arteries.

Two secondary safety signals deserve attention. Silent cerebral lesions, detected on brain MRI 12 to 48 hours after ablation, appeared in two patients (1.9 percent)—a rate lower than the 6.7 to 12.9 percent reported in some other PFA studies. The lesions disappeared completely on follow-up imaging at three and six months. The authors attribute the low rate partly to their waveform choice, noting that bench tests showed biphasic waveforms generate fewer microbubbles than monophasic ones, and that asymmetric biphasic pulses achieve better ablation depth than symmetric ones. Electrode geometry was also deliberately designed to avoid sharp edges and current-concentration hotspots that promote arcing and bubble formation. Meanwhile, laboratory hemolysis was common—87.6 percent of patients met the prespecified definition, with significant drops in haptoglobin and rises in lactate dehydrogenase and free plasma hemoglobin—but creatinine levels were unchanged and no patient developed acute kidney injury. The authors credit their asymmetric waveform, the basket-type catheter with single-sided electrodes that keeps current focused on tissue rather than blood, and a standardized peri-procedural saline hydration protocol. The study has limitations worth noting: it was single-arm with no comparator, lacked continuous implanted rhythm monitoring, enrolled a relatively modest sample, and excluded patients with significant renal impairment, so the hemolysis findings may not generalize to that population. Still, as a real-world, multicenter demonstration that a re-engineered pulse waveform and catheter geometry can deliver complete pulmonary vein isolation with an exceptionally clean safety record, the trial adds meaningful weight to the argument that the next generation of PFA will be defined as much by waveform physics as by catheter design.

Subject of Research: Clinical evaluation of an asymmetric biphasic pulsed field ablation system for paroxysmal atrial fibrillation

Article Title: Asymmetric biphasic pulsed field ablation of paroxysmal atrial fibrillation: clinical assessment

Article References: Xu, X., Li, Y., Lu, F., Li, H., & Cai, H. (2026). Asymmetric biphasic pulsed field ablation of paroxysmal atrial fibrillation: clinical assessment. Frontiers in Cardiovascular Medicine, 13, Article 1945178. https://doi.org/10.3389/fcvm.2026.1945178

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1945178

Keywords: pulsed field ablation, atrial fibrillation, pulmonary vein isolation, irreversible electroporation, biphasic waveform, silent cerebral lesions, hemolysis, coronary vasospasm, cardiac electrophysiology, catheter ablation, clinical trial, Tianjin Medical University

The patient’s story began with two years of troubling palpitations. When his heart raced, an electrocardiogram captured an irregular narrow-complex tachycardia at 111 beats per minute, complete with right bundle branch block morphology and a leftward axis deviation of minus 21 degrees. Yet his heart was structurally sound: transthoracic echocardiography showed preserved left ventricular function and no abnormalities, and his thyroid function was normal. High-resolution, contrast-enhanced computed tomography revealed a crucial anatomical detail that would later prove decisive. His left superior and left inferior pulmonary veins did not drain into the left atrium separately, as they do in most people. Instead, they formed a single left common pulmonary vein, a variant present in a minority of the population that creates a wider, more complex target for any ablation strategy.

His first procedure was, by every conventional measure, a textbook success. Under general anesthesia with propofol and fentanyl, ventilated through a supraglottic i-gel airway, he underwent pulsed field ablation using the FARAPULSE system from Boston Scientific. The team delivered twenty-two applications to the left common pulmonary vein, ten to the right superior vein, and eight to the right inferior vein, alternating between the device’s basket and flower electrode configurations. Each application used a 2.0 kilovolt biphasic waveform with four pulse trains, and catheter contact was verified before every delivery using fluoroscopy and intracardiac echocardiography. When the team finished, electro-anatomical mapping with the EnSite NavX system confirmed that all the pulmonary veins had been acutely isolated from the left atrium. The electrical triggers responsible for his arrhythmia appeared, on the maps, to be sealed off for good.

Three months later, an external event monitor told a different story. Atrial fibrillation had returned. The team brought him back for a second procedure, this time with an esophageal temperature probe in place and access gained through the right internal jugular and right femoral veins. Using the OctaRay mapping catheter and the CARTO3 v8 system from Biosense Webster, they began reconstructing the arrhythmia in three dimensions. Almost immediately, they caught something valuable in the act: spontaneous premature atrial contractions, the stray beats that ignite atrial fibrillation, firing on the monitor in real time. Mapping placed their origin just beneath the ostium of the left common pulmonary vein on the posterior wall of the left atrium, slightly apart from the isolation line created during the first procedure.

What followed was a genuine detective story played out with millimeter precision and millisecond timing. Radiofrequency applications with a QDOT Micro catheter at 35 watts and a target ablation index of 400 transiently suppressed the premature beats but could not eliminate them permanently. Meanwhile, voltage mapping during right atrial pacing revealed that the left pulmonary vein had electrically reconnected to the atrium, with ripple mapping pinpointing the anterior carina, the ridge between the vein branches, as the earliest site of reconduction. The puzzle was this: the recurring trigger sat on the posterior wall, far from the isolation line, yet the reconnected vein was waking up first at the anterior carina. The two findings only made sense together if electricity was traveling along a concealed route outside the endocardial surface.

To test that hypothesis, the team paced from four distinct sites inside the left common pulmonary vein and measured how long each impulse took to reach the distal coronary sinus electrode. The numbers were striking. Pacing from the posterior bottom of the vein produced a conduction time of 140 milliseconds, and from the posterior roof 138 milliseconds, while pacing from the anterior ostium produced just 30 milliseconds. When the map was reconstructed with pacing from the vein, the earliest activation site matched the uneliminated trigger exactly. The pattern pointed to an epicardial connection, a subepicardial muscular bundle linking the anterior carina of the left pulmonary vein to the posterior atrial wall near the vein’s ostium, rather than a simple endocardial gap in the ablation line. The team targeted this presumed pathway at the inferior portion of the anterior carina with 35 watts and a target ablation index of 500, completed the pulmonary vein isolation, and rendered the arrhythmia non-inducible.

The anatomical suspect in this case has a name that cardiologists know well: the ligament of Marshall. This vestigial structure, a remnant of an embryonic vein, carries the Marshall bundle of myocardial fibers from the coronary sinus up the epicardial surface between the left atrial appendage and the left superior pulmonary vein. Its fibers can link the coronary sinus, the posterior and lateral left atrial wall, the ridge of the appendage, and the pulmonary vein antrum into a subepicardial conduction network that no endocardial ablation line can interrupt until lesions become fully transmural. Epicardial connections of this kind are not exotic curiosities. Studies estimate they occur in roughly 11 to 14 percent of patients with atrial fibrillation, and they are more numerous in patients with advanced disease and enlarged left atria. High-density mapping studies have shown that most cluster at the pulmonary vein carina and can extend well beyond the antral ablation line, explaining residual vein potentials and preserved atrial capture even when entrance and exit block appear complete.

Here the left common pulmonary vein becomes more than an anatomical footnote. Research by Kueffer and colleagues has found that this vein variant shows the lowest durability after pulsed field ablation, and the reasoning is anatomically elegant. In patients with a left common trunk, the ligament of Marshall lies closer to the ablation target, increasing the opportunity for epicardial fibers to bypass standard lesion sets. Intriguingly, the picture reverses with radiofrequency energy: lower recurrence rates have been reported for left common pulmonary vein patients treated with point-by-point radiofrequency, while the cryoballoon, another one-shot device like FARAPULSE, has shown reduced durability in the same anatomy. The implication is uncomfortable for the newest technology. One-shot ablation devices, which deliver energy in a fixed geometric pattern, may be inherently more vulnerable to anatomical variants than flexible, point-by-point techniques that an operator can adapt lesion by lesion.

The outcome for the patient, at least so far, is encouraging. After the second procedure he took no anti-arrhythmic drugs or beta-blockers, only a single anticoagulant for six months. Over a full year of follow-up, serial 24-hour Holter monitoring and 12-lead electrocardiography found no recurrence of atrial fibrillation, and he remained entirely asymptomatic, with annual Holter monitoring planned thereafter. The authors are candid about the limits of their evidence. This is a single case that cannot be generalized to everyone with a left common pulmonary vein, and because no electrode catheter was placed within the epicardial pathway and no ethanol was infused into the vein of Marshall, the exact route of the connection was inferred from post-pacing intervals rather than directly proven. The endocardial latency gap, a phenomenon in which conduction recovers with delayed timing, could not be definitively excluded, though the successful ablation at the anterior carina strongly supports the epicardial explanation.

Even with those caveats, the case lands at a consequential moment. Pulsed field ablation is expanding rapidly across the world on the strength of high acute isolation rates and a favorable early safety profile, sparing the esophagus and phrenic nerve from the collateral injury that thermal energy sources can cause. But durability, not acute success, is what determines whether a patient is truly cured, and long-term data relative to conventional treatment remain uncertain. The message from this case is that a perfect-looking lesion set on the inside of the heart can be quietly defeated by conduction running along the outside. For patients with a left common pulmonary vein, the authors argue, careful evaluation and explicit consideration of epicardial reconnection should be part of every ablation plan. As pulsed field technology matures, the hearts it fails to fix may teach clinicians as much as the ones it heals, and the answers may lie in structures no catheter can see from within.

Subject of Research: Epicardial connection as a mechanism of atrial fibrillation recurrence after pulsed field ablation

Article Title: Epicardial Connection as a Resource of Atrial Fibrillation Recurrence After Pulsed Field Ablation: A Case Report

Article References: Lee, K. H., Kitamura, T., Sahashi, S., Sugiyama, H., Izumi, C., & Hayashi, K. (2026). Epicardial Connection as a Resource of Atrial Fibrillation Recurrence After Pulsed Field Ablation: A Case Report. Clinical Case Reports, 14(10), Article e73282. https://doi.org/10.1002/ccr3.73282

Image Credits: AI Generated

DOI: 10.1002/ccr3.73282

Keywords: atrial fibrillation, pulsed field ablation, epicardial connection, pulmonary vein isolation, ligament of Marshall, left common pulmonary vein, electroanatomic mapping, cardiac electrophysiology, FARAPULSE, arrhythmia recurrence, case report, ablation durability