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: I'm Doctor. Sharma and welcome back to EP Edge Journal Watch. Thank you for the feedback, trial suggestions and questions. They genuinely shape what makes it into the show and how we frame it. This episode deserves a focused twenty five minutes because it moves from the electrode tissue interface to ventricular activation and arrhythmia termination and then upstream to sleep, fitness, and lifetime cardiovascular risk.
You finish a PFA case, every pulmonary vein is isolated and the acute result looks perfect. But you've had this thought before: will it still be perfect when the patient comes back months later? That's the problem behind the VISION F. F. B study.
PFA can create fast, relatively tissue selective lesions, but the field still has to reach the myocardium at the right intensity. Most systems ask you to infer contact from shape, fluoroscopy, intracardiac echo, impedance or force. Useful signals: yes. Direct proof: no. So what happens when the operator can actually see the electrode touching tissue before delivering energy?
Fifty patients with symptomatic paroxysmal atrial fibrillation underwent a first ablation at one center. The balloon carried 12 ablation electrodes and an integrated endoscope, and most patients returned for invasive remapping at roughly three months. Rhythm follow-up continued through six months. Here's the headline: Durable isolation was present in ninety nine point four percent of remapped pulmonary veins. In plain terms, the acute lesion set almost completely held up when the veins were checked again.
Per vein durability and patient level durability answered different questions. A single reconnected vein means a patient no longer has complete durable isolation. The patient level result was also very strong, which is why this feasibility study is hard to dismiss. My read is that the innovation may be larger than the balloon. It's a procedural philosophy: verify contact rather than assume it.
But this was a selected first in human cohort with expert operators, early remapping, and no established PFA Exceptional feasibility isn't proven superiority. Does this change my practice? Not yet. It does make direct visualization worthy of a randomized, multicenter comparison with rigorous remapping and longer rhythm surveillance. The full remapping data, procedural figures and safety details are in the EP Edge Journal Watch newsletter.
Now picture a different PFA case. The veins are isolated but the urine turns dark. Creatinine rises the next morning and discharge is no longer routine. What looked like a laboratory signal has become a clinical problem. PFA can disrupt red blood cells inside the blood pool.
Free hemoglobin reaches the kidney, where dehydration, low pressure, renal disease, and a larger energy burden can combine into pigment related injury. The unresolved question was how often acute kidney injury follows, who is vulnerable, and whether structured hydration helps. The investigators followed five zero one consecutive patients treated with a pentaspline system. Earlier procedures had no predefined hydration plan. Later procedures used at least two liters of normal saline around the case, adjusted when congestion was a concern, and creatinine was checked the next day.
Acute kidney injury occurred in nine point nine percent without protocol hydration and three point three percent with it. That's a meaningful difference, but it doesn't prove the fluid protocol caused all of it, because the groups came from different treatment eras. The deeper signal was dose. Patients with kidney injury received more applications, and chronic kidney disease narrowed the apparent margin further. Pulse count isn't just a generator number.
It behaves like a biologic dose. The cohort derived pulse thresholds aren't universal safety cutoffs. They describe this platform, this workflow, and these patients. Hydration may expand the margin. It shouldn't become permission for unlimited applications.
Here's my Monday morning take: Know the baseline creatinine, think through the pulse budget, and pause before extensive extrapulmonary vein ablation. Hydration should be deliberate, not automatic. A patient with heart failure may need less fluid, slower delivery, or diuretic support. After a high pulse count, visible hemoglobinuria, hypotension, or chronic kidney disease, checking creatinine is basic surveillance. The pulse count curves, hydration protocol, and renal safety pathway are laid out in the full newsletter.
Now move back into the lab, to a moment every operator recognizes. Energy is delivered, the patient coughs, the arterial tracing collapses, and the heart rate may barely change. Is this sedation pain, a vagal event, or a direct autonomic response to PFA? Circular array PFA can trigger cough, bradycardia, atrioventricular block, sinus arrest, or hypotension. Routine cuff measurements can miss the speed and depth of the response.
The sequence of vein treatment may matter too. This analysis used beat to beat radial arterial pressure in the first fifty patients treated with a Pulse Select system. Each application was linked to location, order, cough, and rhythm response. Treatment sequence wasn't randomized, it evolved with local experience. Seventy six percent of patients had at least one predefined blood pressure drop.
That doesn't mean every application was unstable. Only a minority of individual applications caused a drop, yet most patients had at least one. That's the difference between application level and patient level risk. The highest risk period was the opening vein, with risk attenuating as the sequence progressed. Distal applications carried more risk, and severe events clustered more on the left side.
Cough often traveled with the pressure drop, but a rhythm defined vagal response did not. A stable heart rate does not guarantee stable hemodynamics. My practical read is straightforward: in a patient with poor ventricular function, pulmonary hypertension, significant valve disease, or marginal starting pressure treat the first pulmonary vein as the high alert phase, use reliable pressure monitoring, have vasoactive support and pacing capability ready before energy delivery. This does not prove that a right vein first sequence is superior. It does tell us that sequence is a modifiable procedural variable worth testing rather than treating as habit.
The application level data and autonomic graphic are available in this issue of EP Edge Journal Watch. A different sequence problem comes next. Not the order of pulmonary veins, but the order in which the ventricle activates for years after a pacemaker implant. Right ventricular pacing is dependable and familiar. It is also electrically non physiologic.
With a high pacing burden, altered activation can drive dyssynchrony, adverse remodeling, worsening mitral regurgitation, atrial fibrillation, and heart failure. What we have lacked is randomized preventive evidence in patients who haven't yet developed pacing induced cardiomyopathy. PACE-HF asked whether LBP pacing could preserve ventricular function better than conventional right ventricular pacing. One hundred and twenty adults with a left ventricular ejection fraction above 40% and an expected substantial pacing burden were randomized at a single center. They received either right ventricular pacing or left bundle branch area pacing, and a blinded core reader assessed ejection fraction after twelve months.
The main result was a left ventricular ejection fraction of fifty seven percent with left bundle branch area pacing versus forty eight percent with right ventricular pacing. The meaning isn't simply that one group improved, it's that non physiologic activation produced measurable deterioration over only a year. There was a procedural price. Conduction system pacing took more implant time, more fluoroscopy, and more expertise. The trial was small, single center, and powered around ventricular function rather than clinical events.
The heart failure hospitalization signal pointed the same way, but the trial wasn't sized to settle it. It also grouped true left bundle capture with left ventricular septal and deep septal pacing, so the exact active ingredient remains blurred. Still, this moves the needle. For a patient expected to be paced most of the time, my default question is increasingly why choose chronic dyssynchrony and wait to see whether the ventricle tolerates it? That doesn't mean every low burden pacemaker needs a conduction system lead.
It means anticipated pacing burden should influence implant strategy. The complete pacing, remodeling and hospitalization data are in the written EP Edge Journal Watch Issue. Now take that same idea, engaging the conduction system, and apply it to ventricular tachycardia therapy. Anti tachycardia pacing has traditionally been treated as a timing problem. You adjust coupling interval, percentage of tachycardia cycle length, pulse count and number of attempts, but the pulse still usually starts at the right ventricular defibrillator lead.
We rarely ask whether the pacing site itself limits success. Right ventricular pacing enters working myocardium and spreads largely cell to cell. Pacing from the left bundle branch area may recruit the Purkinje network sooner and distribute the wavefront more broadly. Can the same therapy work better when it starts from a more strategic location? This was a canine ischemia reperfusion model.
Six animals were analyzable, repeated VT episodes were induced, and episodes received either left bundle branch area or right ventricular apex antitachycardia pacing. Basket mapping tracked how quickly the paced wavefront overtook the tachycardia sequence. VT terminated in seventy point two percent of episodes with LBP versus forty seven point three percent with right ventricular pacing. The confidence interval stayed just above one, so the result met statistical significance but only narrowly. Mapping supported the mechanism.
The Purkinje system and working myocardium activated earlier from the conduction system site. Here's the caveat: these weren't independent patients with spontaneous scar related VT. They were repeated induced episodes in six animals, four days after an experimental infarction. A clustering model can't turn a small biological sample into a large one. My take isn't to implant an extra lead solely for anti tachycardia pacing.
That's premature. But patients who already have a conduction system pacing lead and defibrillation capability offer a logical path to a human crossover trial, randomizing spontaneous episodes between sites and measuring termination, acceleration, shocks, symptoms, and time to success. For the activation maps and episode level details, use the full newsletter alongside this audio discussion. After myocardial infarction, ventricular arrhythmia isn't only a scar problem, it's an autonomic problem too. Sympathetic activation rises, refractoriness destabilizes, triggered activity increases, and an injured ventricle becomes easier to provoke.
Stellate ganglion block and cardiac sympathetic denervation can interrupt that physiology, but they are invasive and not suited to every patient. Spinal cord stimulation is adjustable and potentially reversible, yet prior cardiovascular work has been mixed, and conventional stimulation may cause uncomfortable paresthesia. Could a pulsed UFW reduce post infarction arrhythmia vulnerability without damaging neural structures. 20 pigs were divided among control, untreated myocardial infarction and myocardial infarction plus stimulation groups. Bilateral leads were placed from T1 through T3.
Treated animals received stimulation twice daily for one month, followed by rhythm monitoring, autonomic assessment, electrophysiology testing and neural histology. VF inducibility was one hundred percent after untreated infarction versus twenty nine percent with stimulation. That's a large difference in experimental vulnerability. It isn't the same as preventing spontaneous sudden death in a patient. Lower PVC burden and a coherent autonomic signal pointed the same way, while neural tissue showed no substantial structural injury.
The restraint is obvious this was a small animal pilot without sham implantation, full contemporary post infarction therapy, or spontaneous clinical events. Even the apparent ejection fraction improvement didn't produce a statistically significant final difference between treated and untreated infarct groups. A within group improvement can look persuasive, but the treatment question depends on the between group comparison. My read is that the niche is plausible, more durable than a temporary block, less permanent than denervation, and adjustable over time, but the next step remains preclinical, with sham control, chronic scar, standardized infarct burden, spontaneous monitoring and longer follow-up. Now we leave the Procedure room and move upstream.
A patient with atrial fibrillation tells you they sleep badly. Maybe they can't initiate sleep. Maybe they wake repeatedly. Maybe alcohol has become the nightly solution. We routinely ask about sleep apnea but insomnia often gets filed under quality of life rather than arrhythmia risk.
The biology is plausible. Insomnia can increase sympathetic tone, worsen blood pressure and metabolism, amplify inflammation and make exercise and weight control harder. The problem is confounding. Insomnia travels with anxiety, depression, sleep apnea, medication exposure, chronic illness, and more health system contact. The investigators used a nationwide Japanese database of 1,780,764 adults without prior cardiovascular disease or atrial fibrillation.
Median follow-up was three point seven years. Clinically coded insomnia was compared with no insomnia, with adjustment for major demographic, metabolic, sleep, and lifestyle factors. After adjustment, insomnia was associated with a hazard ratio of one point one four for incident atrial fibrillation. That means the diagnosed insomnia group had about a fourteen percent higher rate of new atrial fibrillation over follow-up. It doesn't mean fourteen percent developed atrial fibrillation and it doesn't prove insomnia caused it.
The association is modest. Much of the raw difference disappeared after adjustment, showing that age, comorbidity, sleep apnea, and lifestyle explained a large part of the signal. The limitation is the exposure itself. Administrative codes can't tell you severity, duration, sleep length, treatment response, or how much undiagnosed sleep apnea remained. Greater healthcare contact could also increase atrial fibrillation detection.
Does this change practice? It doesn't make insomnia a stand alone predictor. It makes insomnia a useful door into the upstream substrate. Ask about apnea: alcohol used as a sleep aid, blood pressure, anxiety, depression, shift work, physical inactivity, and treatment adherence. Treat the cluster, not the billing code.
Exercise creates a different counseling problem. A highly fit patient develops atrial fibrillation and asks the question you know is coming: Did all this training hurt my heart? The answer can't be reduced to a slogan: High fitness and endurance exposure may increase atrial fibrillation risk through atrial enlargement, autonomic adaptation, repeated volume loading, inflammation or fibrosis. At the same time, fitness lowers ischemic disease, stroke, heart failure, metabolic disease, and premature death. Fitness and atrial fibrillation also have familial components.
Shared genes and family environment can make fitness look more causally linked to atrial fibrillation than it is. This Swedish cohort followed men who completed military conscription testing at about age 18. Fitness came from a maximal bicycle test and outcomes were tracked for decades. A large full sibling analysis partially controlled for shared genetic and environmental factors. By age 65, the sibling analysis showed an approximate 1.6 percentage point net cardiovascular benefit associated with high adolescent fitness despite the excess AFib signal.
The broader reduction in non atrial fibrillation cardiovascular disease was larger than the added AFib risk. The AFib excess didn't disappear. It simply didn't outweigh the broader benefit. An apparent early net disadvantage in the overall population disappeared when brothers were compared with brothers. That doesn't eliminate every confounder.
Siblings differ in smoking, alcohol, training, body composition, and many other exposures, but it weakens a purely harmful interpretation of high fitness. The biggest limitation is exposure measurement. Fitness was tested once in adolescence. The study couldn't identify lifelong endurance athletes, changes in training, recovery patterns, or atrial remodeling. It included men only.
My practical message is balanced. Don't tell patients that exercise associated atrial fibrillation is imaginary. Recognize it early. Assess training load and recovery. Address alcohol, sleep, hypertension and body composition, and individualize the plan, but don't undermine the broader cardiovascular value of fitness.
The net signal remained favorable. The age specific curves and sibling comparisons are shown in the written issue. That brings us to the last study which asks not whether people should move but how the intensity should be mixed. Guidelines let one minute of vigorous activity count like two minutes of moderate activity. That's a practical energy equivalence rule.
It doesn't prove the physiologic effects are identical. Vigorous exercise may improve fitness, insulin sensitivity, vascular function and autonomic conditioning more efficiently. Moderate activity is more accessible, often safer and easier to sustain. For the same total activity volume, does the balance between moderate and vigorous exercise matter for survival? The analysis used 586,936 United States adults from the National Health Interview Survey linked to mortality records.
Activity was self reported at baseline and median follow-up was ten years. Participants reported moderate activity, vigorous activity, a combination or inactivity. Compared with inactivity, combined moderate and vigorous activity was associated with a hazard ratio of zero point five zero for all cause mortality. That means the combined activity group had about half the rate of death during follow-up after adjustment. It doesn't mean prescribing a mixed program will cut an individual patient's mortality risk in half.
Why not? Because this is observational. People capable of vigorous activity are often healthier and different in ways the model can't capture. Activity was reported once, not measured by a wearable, and reverse causation remains possible. The lowest estimates generally appeared when some activity was vigorous, yet that may reflect sustainability or healthy user effects as much as physiology.
That distinction matters because the data don't support an all vigorous prescription. The apparent optimum was a mixture. Here's the clinical translation: Moderate activity remains highly beneficial. Don't turn vigorous exercise into a requirement for someone who can't do it safely or consistently. For a capable patient, build regular moderate volume then add vigorous intervals when appropriate.
In electrophysiology that prescription still has to respect atrial fibrillation phenotype, ventricular function, ischemic disease, medication response, symptoms, and prior ventricular arrhythmia. The mortality hierarchy and intensity mix graphic are in the complete newsletter. Let's pull the episode together. Direct visualization during PFA produced remarkable pulmonary vein durability. The signal demands a comparative trial but doesn't declare a winning platform.
The renal study turns pulse count into a safety variable. Plan the dose, respect chronic kidney disease, individualized fluid, and monitor patients with a high procedural burden. The pressure analysis makes the opening pulmonary vein the high alert phase of circular array PFA. Watch pressure, not just rhythm, and have support ready before the first application. Pace.
HF adds randomized evidence that physiologic activation can preserve ventricular function when pacing burden is substantial. The implant effort is immediate. The cost of dyssynchrony accumulates quietly. Conduction system antitachycardia pacing opens a spatial dimension in VT therapy. It isn't ready for routine implantation decisions, but it is ready for a careful human crossover study in patients who already have the hardware.
Pulsed ultra high frequency spinal cord stimulation reduced post infarction arrhythmia vulnerability in an animal model. The concept is compelling, but sham controlled chronic testing has to precede clinical enthusiasm. Insomnia carried a modest independent association with new atrial fibrillation. Its best current use may be prompting a broader conversation about apnea, alcohol, mental health, blood pressure, and activity. High adolescent fitness retained a net cardiovascular benefit after sibling adjustment, despite an atrial fibrillation excess.
Counsel the athlete honestly, treat the arrhythmia, and preserve the value of exercise. The activity intensity study reinforces a practical progression: move regularly, build sustainable volume, and add vigorous work when it can be done safely. The best prescription improves fitness without ignoring substrate or symptoms. All references and graphics are available through the LinkedIn newsletter, EP Edge Journal Watch and on Substack at epedge. Substack dot com.
Questions, suggestions or concerns can be sent to epedge Castgmail . com. Thank you for spending this time with me and for continuing to shape the show with your feedback. Take care.