Elad Anter։ A New Map of Atrial Fibrillation Initiation

Elad Anter, Founder and Chief Scientific Advisor at PhysioMap Ltd., shared a post on LinkedIn about recent articles he and his colleagues co-authored, adding:

”Hot off the press: We identified how and where AF begins.

I am excited to share this work.

Since the landmark discovery of PV triggers more than 25 years ago, AF ablation has evolved into a largely empiric therapy centered on PVI.

Yet, we have never been able to identify the patient-specific arrhythmogenic substrate that determines why a premature beat initiates AF at one site and not another.

We believe this study changes that.

In this mechanistic study, we found that AF initiation arose predominantly through reentry originating from a small number of spatially discrete regions with steep repolarization gradients.

Their distribution was unique to each patient, and they accounted for more than 92 percent of AF initiation episodes.

Importantly, the arrhythmogenic substrate was not defined by low voltage, and while conduction abnormalities were often present, they appeared to play a secondary role.

Its patient-specific distribution may help explain the controversy surrounding posterior wall isolation: the posterior wall harbored the substrate in only approximately 30 percent of patients.

Importantly, in redo patients with durable PVI, right-atrial substrate (which is often beyond standard mapping strategies) was identified in 30 percent.

Most encouragingly, in an exploratory cohort of 24 patients with recurrent AF and durable PVI (50 percent PerAF), targeted elimination of these sites achieved 87.5 percent single-procedure freedom from any atrial tachyarrhythmia over a median of 489 days, without antiarrhythmic drugs.

The thoughtful accompanying editorial by Jon Kalman highlights the significance of this discovery and its central translational challenge of bringing it into real-world clinical practice.

But stay tuned!

Technology is under development to transform this discovery into a rapid, automated functional mapping.

Current electroanatomic mapping relies largely on voltage amplitude and activation timing.

We need to move beyond these measures and map how tissue actually functions – how it conducts, repolarizes, and responds to premature stimulation.

This can add the critical dimension that has long been missing from substrate mapping and may reveal what truly makes cardiac tissue arrhythmogenic.

To me, this is the beauty of physiology: there are no black boxes.

We can identify the sites that reproducibly initiate the arrhythmia, define their EP properties, eliminate them with ablation, and confirm that arrhythmia can no longer be initiated.

The next steps are prospective multicenter validation and technological development.

Together, they may move AF ablation beyond empiric therapy toward truly individualized, mechanism-guided therapy.”

Title 1: Steep Repolarization Gradients: Mapping Where Atrial Fibrillation Begins

Authors:  Udit Thakur and Jonathan M. Kalman

Read the Full Article on JACC: Clinical Electrophysiology

Title 2: Atrial Fibrillation Initiation Arises From Reentry at Patient-Specific Regions With Steep Repolarization Gradients Identified During Sinus Rhythm

Authors: Elad Anter, Michael Barkagan, Dor Yadin, Maxime Zabern, Sivan Hay, Anat Milman

Read the Full Article on JACC: Clinical Electrophysiology

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