Niraj Sharma: Welcome back to EP Edge Journal Watch. This is issue number eight, January 2026. I'm doctor Neeraj Sharma, cardiac electrophysiologist, and the editor and creator of EP Edge Journal Watch. If you've been listening regularly, thank you. I genuinely appreciate you coming back.
A lot of time goes into reading, reviewing and thinking through these studies and the goal is always the same to make the data useful when you're taking care of patients. And if this is your first time listening, welcome. EPH journal watch is where we slow down, look carefully at the numbers and talk honestly about what these trials really show and just as importantly what they do not. Let's start with one of the most difficult clinical situations we face as electrophysiologist, ventricular tachycardia storm. A large multicenter retrospective cohort examined outcomes in patients admitted with VT storm across six high volume tertiary centers spanning nearly a decade.
The total population included sixteen seventy five patients. Of those patients, three sixty three died before hospital discharge. That translates to an in hospital mortality rate of about twenty two percent. That number alone reframes the conversation we have with families. The investigators set out to answer a practical question, can we predict which patients are unlikely to survive the hospitalization and are there modifiable factors that matter?
They developed what they call the CHAMPS risk score derived using multivariable logistic regression with internal validation using bootstrap resampling. The model's discrimination was reasonable with an area under the curve of approximately 0.77 and optimism corrected performance around 0.76. What is striking is not just the model performance but the variables that drove risk. The strongest predictors of in hospital death were markers of systemic illness, acute stroke, hypoxia requiring intubation, sepsis or fever, severe malnutrition, and the use of multiple vasopressor medications. Importantly, an admission diagnosis other than ventricular tachycardia also carried significant risk.
These are not subtle electrophysiology variables, they are indicators that the patient's physiology is already failing. When patients were stratified by CHAMP score, mortality separated clearly. Low risk patients, that's a score of zero, had in hospital mortality around six to seven percent. Intermediate risk patients approached twenty seven percent, high risk patients a score of greater than 10 had mortality exceeding sixty percent before discharge. Now let's talk about intervention.
Catheter ablation was performed in about fifty nine percent of patients overall. Timing mattered. Patients who underwent ablation within seven days of admission had an in hospital mortality of approximately three percent. Those who underwent ablation after seven days had mortality exceeding forty percent. In adjusted analyses, early ablation was independently associated with lower odds of in hospital death while each incremental increase in CHAMP score was associated with a higher mortality risk.
A time varying survival analysis showed a similar association favoring ablation. This does not prove causation. Patients stable enough to undergo early ablation may already be different but the signal is strong enough that it cannot be ignored. The EP edge takeaway is this, ventricular tachycardia storm mortality is often not purely arrhythmic mortality. It is frequently systemic illness mortality but when ventricular tachycardia is the dominant problem waiting to intervene may be a mistake.
Once multi organ dysfunction takes over even perfect arrhythmia control may not change the outcome. That balance between benefit and unintended harm leads directly into the next topic where life saving therapy itself can create significant morbidity, inappropriate shocks from implantable defibrillators. Once we intervene in high risk arrhythmia patients, we expect implantable defibrillators to save lives, but we also know that inappropriate shocks can carry a real physical and psychological burden. A patient level meta analysis combined data from two randomized trials, Praetorian and ATLAS, comparing subcutaneous defibrillators with traditional transvenous systems. These were patients with an indication for a defibrillator but no need for pacing.
The pool population included thirteen forty two patients with a median age of 58 years, about twenty two percent were women and roughly seventy eight percent were implanted for primary prevention. Median follow-up was approximately three and a half years. The primary endpoint was time to first inappropriate shock. Overall the subcutaneous system was associated with a higher risk of inappropriate shock. Event rates were about two point five per one 100 patient years compared with one point five per one 100 patient years for transvenous systems.
The hazard ratio for first inappropriate shock was approximately 1.6, but the real insight comes from understanding why these shocks occurred. Inappropriate shocks were categorized into three mechanisms: cardiac over sensing, interference from muscle activity or electromagnetic signals, and atrial arrhythmias such as atrial fibrillation or SVT. Cardiac over sensing was significantly more common with subcutaneous systems driven by T wave and P wave over sensing. Interference related shocks were also more frequent. In contrast, inappropriate shocks due to atrial arrhythmias were less common with subcutaneous systems than with transvenous defibrillators.
Programming differences matter here. Detection zones, the availability of anti tachycardia pacing and device era all influence outcomes. This was not a perfect head to head comparison of identical technology. The EPH takeaway is practical rather than ideological. Subcutaneous systems reduce lead related complications but they demand meticulous screening and attention to sensing.
Transvenous systems may be quieter in patients with atrial arrhythmias but they carry long term lead risks. Device selection is not about which system is better, it is about which trade offs are acceptable for the patient in front of you. That concept, that arrhythmia outcomes are driven by more than anatomy alone brings us naturally into atrial fibrillation and autonomic modulation. We often describe atrial fibrillation as a pulmonary vein problem but that explanation is incomplete. Autonomic tone and neurohormonal activation play a significant role.
A randomized sham controlled pilot trial explored whether renal sympathetic denervation performed at the time of first atrial fibrillation ablation could reduce arrhythmia recurrence. Patients underwent a technically successful ablation first with pulmonary vein isolation confirmed. Only then were they randomized to renal denervation or a sham procedure. The final analyzed cohort included 100 patients across nine centers. Mean age was approximately 66 years and about thirty five percent were women.
Most patients had paroxysmal atrial fibrillation with a smaller persistent atrial fibrillation subgroup. Ablation modality was mixed including both radiofrequency and cryoballoon techniques. The primary endpoint was freedom from atrial fibrillation or atrial flutter lasting at least thirty seconds at twelve months off antiarrhythmic drugs following a ninety day blanking period. At one year, freedom from atrial arrhythmia was approximately forty nine percent in the sham group compared with sixty seven percent in the renal denervation group. The difference favored renal denervation, but it did not reach statistical significance.
Adjusted analyses showed a hazard ratio favoring renal denervation but confidence intervals were wide. Importantly, no renal denervation related serious adverse events were reported. The EP EDGE takeaway is nuanced. The direction of effect is clinically meaningful and biologically plausible, but this was a pilot study, not a definitive trial. This work supports further investigation, not routine adoption.
It reminds us that atrial fibrillation recurrence is often a substrate problem, not simply a lesion set problem. That substrate becomes even more relevant when we talk about sleep apnea. Let's spend a little more time on atrial fibrillation substrate because this is where a lot of our long term outcomes are actually determined. A large retrospective cohort study used a federated electronic health record network to examine outcomes in patients with both atrial fibrillation and obstructive sleep apnea. The data set spanned nearly a decade and included multiple health systems.
Before any matching, more than one hundred thousand patients carried diagnoses of atrial fibrillation and sleep apnea. Of those approximately nine thousand underwent catheter ablation. After one to one propensity score matching, the final analysis included nine thousand one hundred and sixty two patients in the ablation group and an equal number in the non ablation group. Matching accounted for demographics, cardiovascular comorbidities, and medication use. Follow-up extended out to five years beginning three months after atrial fibrillation diagnosis to minimize immortal time bias.
The outcomes reported were broad. All cause mortality, heart failure hospitalization, ischemic stroke, and a composite of major adverse cardiovascular events. Across these endpoints, catheter ablation was associated with lower event rates. Mortality in particular appeared significantly reduced in the ablation group. Now this is where experienced electrophysiologists need to pause.
The magnitude of mortality benefit observed in this study is larger than what we typically see in randomized atrial fibrillation ablation trials. That discrepancy should immediately raise concern for residual confounding. Healthier patients are more likely to be referred for ablation. They're also more likely to adhere to therapy, have better access to care, and carry fewer unmeasured comorbidities. There's also a major limitation that cannot be ignored.
The data set lacks granular information on sleep apnea severity and adherence to positive airway pressure therapy. We know from prior randomized and mechanistic studies that untreated sleep apnea increases atrial fibrosis, atrial stretch, and recurrence after ablation. Without knowing who was actually treated, causality becomes impossible to establish. The EPH takeaway here is not that ablation saves lives in sleep apnea patients. The real message is that sleep apnea is a powerful modifier of atrial fibrillation outcomes.
Ablation may help, but durable success likely depends on treating the underlying substrate. Now let's shift gears to a more immediate bedside level question that many of us encounter regularly. How do we safely control heart rate in atrial fibrillation with rapid ventricular response, especially in patients with borderline blood pressure? A randomized double blind placebo controlled trial addressed this question. Two seventeen adult patients presenting with atrial fibrillation or atrial flutter and a heart rate greater than 120 beats per minute were enrolled in the emergency department.
Patients were randomized to one of three strategies, placebo pretreatment followed by intravenous diltiazem, pretreatment with ninety milligrams of calcium chloride followed by diltiazem or pretreatment with one hundred and eighty milligrams of calcium chloride followed by diltiazem. Blood pressure and heart rate were measured at baseline and then at five, ten, fifteen minutes after diltiazem administration. The primary physiologic signal was preservation of systolic blood pressure. Patients receiving calcium pre treatment experienced less hypotension particularly at the ten and fifteen minute time points. Importantly calcium pre treatment did not impair early rate control.
The treatment for additional diltiazem dosing and short term heart rate reduction were similar across all three groups. There was no signal of increased adverse events, including no access bradycardia, no high grade AV block, and no short term ischemic complication. The EPH takeaway is not that everyone should receive calcium. This is a targeted strategy. In older patients, those with limited hemodynamic reserve or situations where hypotension might push clinicians towards amiodarone, calcium pretreatment may preserve blood pressure without sacrificing rate control.
And with that practical transition from substrate to bedside management, we can move to the final topic, empowering patients to terminate supraventricular tachycardia outside the hospital. For decades SVT management has lived at two extremes, vagal maneuvers at home or intravenous therapy and ablation in the hospital. A randomized double blind trial evaluated intranasal etrifamil as patient administered therapy for paroxysmal supraventricular tachycardia. Patients were randomized to intranasal etripamil seventy milligrams or placebo used after attempted vagal maneuvers. A second dose was permitted at ten minutes if symptoms persisted.
The primary endpoint was conversion to sinus rhythm within thirty minutes sustained for at least thirty seconds. Conversion occurred in approximately sixty four percent of patients receiving etripamil compared with thirty one percent receiving placebo. Median time to conversion was about seventeen minutes with etripamil versus fifty three minutes with placebo. The number needed to treat was approximately three. No drug related serious adverse events were reported.
The most common side effects were local nasal symptoms. The EPH takeaway is important. This does not replace catheter ablation but for selected patients it offers autonomy, reduces emergency visits and changes how we think about arrhythmia care delivery. And that brings us to the close. Thank you for listening to EP Edge journal watch issue number eight.
All detailed analyses, figures and references are available in the LinkedIn EP Edge journal watch newsletter. One final announcement, toward the January 2026, EP Edge will release a deep data driven analysis of pulse field ablation published as a LinkedIn EP Edge newsletter and paired with an EP Edge podcast episode. Until next time, stay thoughtful, stay data driven, and take care.