AVNRT Ablation: Minimizing Recurrence and Improving Outcomes

Atrioventricular nodal reentrant tachycardia (AVNRT) is a common form of supraventricular tachycardia, often causing palpitations, dizziness, or even syncope. While not typically life-threatening, frequent episodes can significantly impact a patient’s quality of life. Catheter ablation is the preferred treatment for recurrent or symptomatic AVNRT, offering high success rates and symptom relief.

Achieving long-term success while minimizing recurrence requires precise diagnosis, careful procedural planning, and appropriate energy selection during ablation. Understanding these factors optimizes outcomes and reduces complications.

Mechanisms Involved In AVNRT

AVNRT arises from a reentrant circuit within or near the atrioventricular (AV) node, facilitated by dual AV nodal pathways—typically a slow and a fast pathway. In most individuals, electrical impulses travel uniformly through the AV node, but in AVNRT, these distinct pathways create a self-sustaining loop of electrical activity.

The slow pathway, located in the posterior-inferior AV node, has a longer refractory period and slower conduction velocity, while the fast pathway, positioned more anteriorly and superiorly, conducts impulses more rapidly but recovers quickly. A premature atrial contraction (PAC) can block conduction in the fast pathway due to its shorter refractory period, forcing the impulse down the slow pathway. By the time it reaches the lower AV node, the fast pathway has recovered, allowing retrograde conduction to the atria. This continuous cycle sustains the tachycardia.

Atypical AVNRT, though less common, follows an inverse pattern where the fast pathway serves as the anterograde limb and the slow pathway conducts retrogradely. This variant often presents with a longer RP interval on electrocardiography, making it harder to distinguish from other supraventricular tachycardias. Multiple slow pathways or variations in conduction properties can further complicate the arrhythmia’s behavior, affecting cycle length, inducibility, and response to vagal maneuvers or adenosine.

Distinguishing AVNRT On Electrophysiology Studies

Electrophysiology (EP) studies confirm AVNRT and differentiate it from other supraventricular arrhythmias by analyzing conduction patterns, response to programmed stimulation, and the effects of pharmacologic agents. Intracardiac electrograms and pacing maneuvers help pinpoint the reentrant circuit’s involvement in the AV node and guide ablation strategy.

A hallmark of AVNRT is dual AV nodal physiology, identified by a sudden increase in the AH interval—typically greater than 50 milliseconds—when atrial extrastimuli are introduced at progressively shorter coupling intervals. This jump in conduction time suggests both a fast and a slow pathway. Once dual physiology is confirmed, tachycardia can often be induced with atrial pacing or premature atrial beats. Typical AVNRT is characterized by nearly simultaneous atrial and ventricular activation, resulting in a short RP interval on intracardiac recordings. This distinguishes it from orthodromic reciprocating tachycardia, which exhibits a longer RP interval due to its reliance on an accessory pathway for retrograde conduction.

Pacing maneuvers provide further confirmation. Ventricular overdrive pacing evaluates the post-pacing interval (PPI) relative to the tachycardia cycle length. A PPI – TCL difference of less than 110 milliseconds suggests AVNRT, as the circuit primarily involves the AV node. Another key finding is the response to His-refractory premature ventricular complexes (PVCs). In AVNRT, a PVC delivered when the His bundle is refractory does not advance the atrial signal, reinforcing retrograde conduction within the AV node rather than through a bypass tract.

Pharmacologic testing with adenosine or AV nodal blocking agents can further support the diagnosis. Adenosine transiently suppresses AV nodal conduction, often terminating AVNRT by interrupting the reentrant loop. If tachycardia abruptly terminates without affecting atrial activity, it strongly suggests an AV nodal-dependent mechanism. Conversely, persistence of atrial activation after termination may indicate an accessory pathway. Isoproterenol can be used when AVNRT is non-inducible at baseline, as it enhances conduction through the slow pathway and facilitates tachycardia initiation.

Anatomical Targets For Ablation

Successful AVNRT ablation requires precise targeting of the slow pathway while preserving normal AV conduction. The slow pathway is typically located in the posterior-inferior AV node, near the coronary sinus ostium and along the tricuspid annulus. This area, known as the “slow pathway region,” is the optimal ablation site due to its role in sustaining the reentrant circuit. Careful mapping ensures effective modification of conduction properties while minimizing the risk of damaging the compact AV node or the fast pathway, which could result in AV block.

The slow pathway lies within the triangle of Koch, bordered by the tendon of Todaro, the tricuspid annulus, and the coronary sinus. Ablation is typically performed at the inferior portion, where slow pathway potentials or fractionated electrograms are often recorded. Identifying these electrograms confirms slow pathway conduction and ensures targeted energy delivery. Some patients may have multiple slow pathway inputs, requiring a broader yet cautious ablation approach to eliminate conduction while avoiding excessive tissue damage.

Fluoroscopy and electroanatomic mapping refine ablation precision. Fluoroscopy provides a general anatomical reference, while advanced mapping systems offer real-time visualization of catheter position and local electrical activity. In some cases, a stepwise approach is necessary, beginning with low-power applications at the posterior septum and gradually moving superiorly if tachycardia remains inducible. The endpoint of ablation is the elimination or significant modification of slow pathway conduction, evidenced by the absence of dual AV nodal physiology or non-inducibility of tachycardia with programmed stimulation.

Types Of Energy Used In Catheter Ablation

Catheter ablation for AVNRT relies on energy sources that modify cardiac tissue to disrupt the slow pathway while preserving normal conduction. Radiofrequency (RF) energy is the most widely used modality, offering controlled thermal injury to targeted regions. RF ablation generates heat through resistive energy transfer, creating lesions that eliminate the slow pathway’s ability to sustain reentry. Temperature-controlled and power-controlled RF settings allow precise lesion formation, typically using power levels between 20 to 40 watts and temperatures capped at 55 to 60°C to minimize collateral damage.

Cryoablation offers an alternative, particularly for patients at higher risk of AV block due to anatomic variations. Unlike RF, which relies on heat, cryoablation freezes tissue to induce cellular injury, allowing for a reversible test phase before permanent lesion creation. This is especially useful when proximity to the compact AV node raises concerns about conduction impairment. While cryoablation has a lower risk of complications, studies suggest slightly higher recurrence rates compared to RF, with long-term success rates ranging from 85% to 92%.

Key Elements Of The Procedural Setup

Optimizing procedural setup for AVNRT ablation involves patient preparation, catheter positioning, and real-time monitoring to enhance safety and efficacy. Proper sedation is essential, as excessive movement affects catheter stability, yet deep sedation or general anesthesia may suppress arrhythmia inducibility. Many electrophysiologists prefer conscious sedation with agents like midazolam and fentanyl, allowing for patient comfort while maintaining autonomic tone, which influences slow pathway conduction.

Vascular access is typically obtained via the femoral vein, with catheters advanced into the right atrium, His bundle region, and coronary sinus for detailed mapping. Once catheters are in place, slow pathway localization is guided by fluoroscopy, electroanatomic mapping, and intracardiac electrograms. The ablation catheter is positioned at the posterior septal region near the coronary sinus ostium, where fractionated electrograms suggest slow pathway conduction. Stability is monitored through impedance and electrogram consistency, as excessive pressure increases complication risk.

During ablation, junctional rhythms indicate effective lesion placement, with a gradual reduction in slow pathway conduction confirming success. Post-ablation testing, including programmed stimulation and isoproterenol infusion, ensures the elimination of inducible AVNRT before concluding the procedure.

Differences From Other Supraventricular Tachycardias

Distinguishing AVNRT from other supraventricular tachycardias (SVTs) is essential for selecting the appropriate treatment. Unlike atrioventricular reentrant tachycardia (AVRT), which involves an accessory pathway outside the AV node, AVNRT is confined within nodal tissue. AVRT typically presents with a longer RP interval and a retrograde P wave following ventricular activation, whereas AVNRT exhibits nearly simultaneous atrial and ventricular depolarization.

Focal atrial tachycardia (AT) can mimic AVNRT but originates from an ectopic atrial site rather than a reentrant circuit. Unlike AVNRT, AT displays a clear P wave preceding each QRS complex and does not terminate with AV nodal blocking agents like adenosine. Atrial flutter, another distinct arrhythmia, features organized macro-reentrant activity with flutter waves on ECG and requires different ablation targets. Recognizing these differences ensures appropriate treatment and reduces recurrence rates.