Niraj Sharma: Hello, Welcome back to EP Edge Journal Watch. I am Doctor. Neeraj Sharma and thank you for joining me today. This is issue nine dated 02/02/2026. Today's issue is focused on one of the toughest problems we deal with in electrophysiology, ventricular tachycardia management, across the full spectrum.
We'll go from non invasive salvage therapy to earlier substrate modification to next generation device architecture, physiologic, leadless pacing, the continued role of antiarrhythmic drugs, and infection prevention. As always, I am going to keep this practical: clinical context, the key results, and a critical appraisal: what's real, what's limited, and what I think actually changes practice. Alright, first up Stereotactic radioablation for refractory ventricular tachycardia, the Stray MIVT trial published in Europace. Before we get into the data, let's pause for a moment and talk about what stereotactic radioablation actually is. In simple terms, this is a way of treating ventricular tachycardia without putting a catheter inside the heart.
Stereotactic radioablation, sometimes called STAR, uses high precision radiation, the same general technology that's been used for years in oncology, to deliver a focused non invasive dose to a predefined arrhythmogenic substrate in the myocardium. The target is not a tumor, the target is the ventricular scar and border zone responsible for sustaining VT. Instead of applying radiofrequency energy from inside the heart, the goal is to modify that substrate from the outside with a single highly targeted radiation treatment. Practically, the VT circuit is mapped indirectly. We fuse electroanatomic mapping information, cardiac CT, cardiac MRI, and sometimes PET imaging to define a target volume that represents the likely VT substrate.
That target is then treated with a single fraction, most commonly 25 gray, delivered with millimeter level precision while trying to minimize exposure to surrounding structures. Now, the clinical context for STRI MIVT is very specific. These are patients with structural heart disease and recurrent VT who are refractory to antiarrhythmic drugs and catheter ablation, basically a no option population. STAR has been an emerging salvage strategy, but one of the major concerns has been coronary vascular injury and delayed radiation toxicity. What makes dry MI VT important is that it didn't just look at VT suppression, it made coronary safety a defining objective, and it did that in a systematic way.
Here's the setup: Prospective, single center. Nineteen patients with recurrent VT who were deemed unsuitable for further ablation. They defined the VT substrate using multimodality imaging and electroanatomic mapping and delivered a single fraction of 25 gray. Now the key methodological strength, what I want you to remember, is the coronary surveillance. They used baseline and longitudinal coronary CT angiography, applied CAD RADS to assess stenosis, and also looked at pericoronary adipose tissue attenuation as a surrogate marker of coronary inflammation.
There was about an eighty one percent reduction in total ICD therapies. A ATP burden dropped from roughly 4.5 to 0.8 episodes per month. Total ICD therapies declined from 4.8 to 0.9 per month. Mild pulmonary or pericardial toxicity occurred in about twenty two percent. One year mortality was thirty three percent, with no deaths attributed directly to STAR.
Coronary outcomes are the headline. No progression in coronary stenosis by CAD RADS, no increase in pericoronary fat attenuation, and no coronary events attributable to radioablation. Critical appraisal, small study, single center, no comparator, and late toxicity cannot be excluded. But in a true salvage population, this shows meaningful VT burden reduction and directly addresses a major safety concern. STAR remains last line therapy, but Straw MIVT strengthens the safety argument in expert hands.
A companion editorial in JAC Clinical Electrophysiology explored mechanisms of radioablation. Early VT suppression, sometimes within days, suggests effects beyond fibrosis alone. Proposed mechanisms include changes in sodium channel expression, kinexin-forty three upregulation, and altered conduction and refractoriness. Mechanistic uncertainty reinforces discipline. STAR should not expand beyond salvage therapy until durability and biological effects are better defined.
Next, VANISH two, a prespecified sub study in JACC. Catheter ablation versus antiarrhythmic drug therapy in ischemic VT, stratified by drug eligibility. Four sixteen post MI patients with sustained VT were stratified by sotalol or amiodrone eligibility, then randomized with intraday. Median follow-up was four point three years. In sotalol eligible patients, the primary endpoint occurred in forty six percent with ablation versus fifty nine percent with SORT law.
Hazard ratio was zero point six four. Ablation reduced ICD shocks and slow VT below detection thresholds. In amiodarone eligible patients, arrhythmic outprints were similar, but extracardiac toxicity remained higher with amiodarone. Ablation clearly outperforms sotalol and competes with amiodarone without long term systemic toxicity. Next, devices: The Modular ATP Study in Circulation, Arrhythmia, and Electrophysiology.
Modular systems combine an S ICD with a leadless pacemaker capable of ATP, aiming to eliminate transvenous lead complications. Two ninety seven patients enrolled, two eighty six received leadless pacemakers. Implant success was one hundred percent and major leadless pacemaker complication free rate approximately ninety seven percent. A TP terminated VT in about sixty seven percent of episodes. VT acceleration occurred in roughly ten percent.
Many so called inappropriate therapies were actually true ventricular arrhythmias misclassified. This is a programming problem, not a feasibility failure. Let's move next to pacing, specifically dual chamber leadless pacing highlighted by the AVAIR Doctor experience published in Europace. Historically leadless pacing has come with a major trade off: freedom from transvenous leads but at the cost of reliable atrioventricular synchrony. AVAIR Doctor is different.
It uses two independent leadless devices, one atrial and one ventricular, that communicate directly with each other to coordinate atrial sensing and ventricular pacing. This was a prospective multicenter experience designed to answer a very practical question: Can dual chamber leadless pacing actually maintain AV synchrony during real world ambulatory conditions? And the answer, at least in the short term, was yes. Mean AV synchrony approached 96.7% of beats, and importantly, synchrony was preserved not just at rest but during daily activity and higher heart rates. This matters because AV synchrony is not a cosmetic endpoint, It directly affects cardiac output, symptoms, and long term heart failure risk.
Now limitations are real. The cohort was relatively small, follow-up was limited, and we don't yet have hard outcomes, heart failure, hospitalization, atrial fibrillation burden, or long term device interactions. But conceptually, this is an important milestone. Dual chamber leadless pacing is no longer theoretical. The question now is durability, scalability, and where this fits relative to traditional transvenous systems.
And that naturally brings us to the next section. Even as devices become more sophisticated, ablation more effective, pacing more physiologic, antiarrhythmic drugs still matter, not as a failure of procedural therapy but as an essential component of arrhythmia care worldwide. This issue highlights an ERHA expert consensus and a companion document in the European Heart Journal focused on modern antiarrhythmic drug use. The key message is not that we need new drugs, it's that we need to use the drugs we already have more intelligently and more safely. The framework proposed is simple but powerful: antiarrhythmic drugs as appropriate backup or complementary therapy.
The documents move beyond the traditional Vaughan Williams classification and emphasize mechanism, patient phenotype, and risk context. There is a strong focus on drug drug interactions, renal and hepatic adjustment, pro arrhythmia risk, and structured monitoring strategies, particularly in patients with heart failure, inherited arrhythmia syndromes, and during pregnancy. This is not flashy work, but it is exactly the kind of guidance that prevents avoidable toxicity and improves long term outcomes. Finally, infection prevention. And this is an important reminder that even small procedural details can have major downstream consequences.
The CLOVIS trial, published in JAAC, examined skin antisepsis strategies specifically in patients undergoing CRT implantation. Over two thousand two hundred patients were randomized to alcoholic chlorhexidine versus a multi step povidone iodine alcohol regimen. Follow-up extended to twenty four months. Infection rates were low in both groups and not significantly different, roughly two point nine percent versus three point nine percent. Skin toxicity was uncommon and similar between groups.
The takeaway here is not that skin prep doesn't matter, it's that skin prep alone is not decisive. Infection prevention is multifactorial. Hematoma avoidance, meticulous technique, patient comorbidities, and post procedural care often matter more than the specific antiseptic used. EPH bottom line for issue nine: Star reduces VT burden without short term coronary injury. Ablation outperforms sotalol in ischemic VT.
Modular ICD systems are feasible. Dual chamber leadless pacing is real. And infection prevention is never just one step. Thank you for spending this time with me. All details for this issue are available on LinkedIn in the EP Edge Journal Watch newsletter.
If you have questions or thoughts reach out to me at epedgecastgmail dot com. I'm Doctor. Sharma. See you in the next issue and bye for now.