The most common regular supraventricular tachycardia encountered in clinical practice is AV nodal reentrant tachycardia (AVNRT). This arrhythmia is relatively rare in childhood with a marked increase in prevalence after puberty. There is a marked female preponderance (in contrast to most other arrhythmias). The clinical symptoms associated with AVNRT are quite variable but are generally dependent on the rate and duration of the tachycardia. Although syncope is not usual, many patients will experience lightheadedness at the onset of tachycardia followed by rapid palpitations and a feeling of pulsations in the neck. Some individuals develop a sensation of chest pressure and dyspnea, especially if the tachycardia is sustained. Termination of the tachycardia is usually abrupt and may be facilitated by vagal maneuvers.
The Mechanism and Electrocardiogram of AVNRT
The mechanism in over 95% of cases of AVNRT involves antegrade conduction over the slow AV nodal pathway with retrograde conduction over the fast AV nodal pathway (slow-fast AVNRT). The electrocardiogram typically demonstrates a regular tachycardia with P-waves that occur simultaneously with the QRS complexes and cannot be visualized. In some cases the terminal portion of the P-wave can be seen to distort the end of the QRS. The PR interval is prolonged due to slow antegrade conduction over the slow AV nodal pathway while the RP interval is very short due to rapid retrograde conduction over the fast AV nodal pathway. In rare cases the reentrant circuit may be reversed with antegrade conduction over the fast AV nodal pathway and retrograde conduction over the slow AV nodal pathway (fast-slow AVNRT). This variant has a characteristic ECG pattern with a P-wave that is inverted in the inferior leads (II, III, and AVF) and upright in leads AVR and AVL. The PR interval is normal (<0.20 sec) as there is rapid antegrade conduction over the fast pathway while the RP interval is long due to slow retrograde conduction over the slow AV nodal pathway. In almost every case there is a 1:1 atrioventricular relationship such that AV block during the tachycardia strongly suggests that an atrial tachycardia rather than AVNRT is the underlying mechanism.
Catheter Ablation of AVNRT
Although either the slow or the fast AV nodal pathways can be targeted for catheter ablation to treat AVNRT, elimination of the slow pathway is the preferred strategy. Catheter ablation is combined with a diagnostic electrophysiologic study in a single session. The diagnostic electrophysiologic study is used to replicate the clinical tachycardia, to define its mechanism, and to exclude the presence of other arrhythmia mechanisms. Indeed, multiple arrhythmia mechanisms such as the presence of an accessory AV pathway, atrial tachycardia, ventricular tachycardia, or atrial flutter may be present in an individual and the accurate definition and treatment of each tachycardia is important.
After intravenous sedation, diagnostic electrode catheters are placed percutaneously in the coronary sinus, across the tricuspid annulus to record His bundle activation, at the right ventricular apex, and in the high right atrium. The properties of AV nodal conduction are then assessed with the technique of programmed electrical stimulation using a catheter in the right atrium. During programmed stimulation, a sequence of 8 paced electrical stimuli is delivered at a constant rate that allows stable AV nodal conduction (the S1 drive). Following these 8 beats, a premature stimulus is delivered (S2) and the resultant atrial to His bundle conduction interval (AH interval) is measured in the His bundle recording catheter. This stimulation sequence is repeated at progressively shorter S1-S2 intervals, allowing the response of the AV node to be recorded across a range of premature test stimuli. A characteristic AV nodal conduction pattern can be demonstrated in patients with AVNRT that suggests the presence of dual AV nodal pathways. In contrast to the normal pattern of AV nodal conduction, in which the AH interval gradually lengthens in response to progressively more premature atrial extrastimuli, patients with AVNRT usually demonstrate a sudden increase in the AH interval at a critical S1S2 stimulation interval. This interval represents the effective refractory period of the fast AV nodal pathway such that the premature stimulus finds the fast AV nodal pathway refractory and proceeds over the slow AV nodal pathway with a marked increase in the AH conduction interval. Patients with AVNRT also demonstrate a characteristic response to rapid atrial pacing, such that the PR interval gradually prolongs as the pacing rate is increased. When a critical pacing rate is reached the PR interval typically exceeds the R-R interval with all AV nodal conduction over the slow AV nodal pathway. If pacing is then abruptly interrupted, AVNRT is often induced.
Typical slow-fast AVNRT is characterized by a prolonged AH interval and a short HA interval. In most cases of slow-fast AVNRT the site of earliest retrograde atrial activation is recorded in the His bundle recording catheter. Rarely, retrograde activation may involve left atrial fibers that insert into the musculature of the coronary sinus with earliest activation recorded at the ostium of the coronary sinus. AVNRT of the fast-slow variety is characterized by a long HA interval with earliest activation of the atrium at the ostium of the coronary sinus. This form of AVNRT is typically induced by ventricular pacing and is rarely induced from the atria. Induction of AVNRT is often facilitated by the intravenous infusion of isoproterenol, especially when the patient is sedated. Once the tachycardia is induced, rapid pacing or premature ventricular stimuli are delivered from the right ventricle to exclude the presence of an accessory AV pathway or atrial tachycardia.
After establishing that the mechanism of the tachycardia is AVNRT, a specialized catheter to be used for ablation is advanced across the inferior portion of the tricuspid annulus. This catheter has a tip electrode measuring 4-5 mm in length and incorporates a thermistor or thermocouple for measuring temperature of the electrode during the application of radiofrequency current. Although there have been several terminologies introduced to indicate the location of the ablation electrode relative to the region of the AV node, a common scheme divides the region of the septal leaflet of the tricuspid valve annulus into 10 sites. The level of the floor of the coronary sinus ostium is labeled site 10, whereas the most superior portion of the annulus recording the largest amplitude of the His bundle potential is labeled site 1. The slow AV nodal pathway is usually ablated at sites 8-10 along a ridge of tissue immediately anterior to the coronary sinus ostium. This ridge of tissue is usually only 4-10 mm in width and includes atrial fibers that are bordered posteriorly by the coronary sinus ostium and anteriorly by the tricuspid valve annulus. The electrogram recorded from the ablation electrode at this site demonstrates a large ventricular potential and a small atrial potential, usually with fractionated deflections. Radiofrequency current is applied for 60-120 seconds at this site with a target temperature of 60 degrees C. The characteristic response to application of radiofrequency current over the slow AV nodal pathway is the development of an accelerated junctional rhythm with intact ventriculo-atrial conduction. Following the application of radiofrequency current, the effect on AV nodal conduction is reassessed using programmed atrial stimulation and rapid atrial pacing. During rapid atrial pacing after successful slow AV nodal pathway ablation, the PR interval will no longer exceed the RR interval before AV nodal Wenckebach block is observed. The typical response to ablation is to eliminate slow AV nodal conduction altogether with conversion of the AV nodal conduction curve from dual pathways to only fast pathway conduction. However, the persistence of a dual AV nodal conduction pattern or the induction of single AV nodal echo beats does not indicate that further ablation is needed as long as AVNRT cannot be induced in the presence of isoproterenol. On the other hand, if 2 or more AV nodal echo beats can be induced, or if the PR interval can exceed the RR interval during rapid atrial pacing, further ablation treatment is needed.
Results of Slow AV Nodal Pathway Ablation
The results of AV nodal ablation are excellent, with most experienced laboratories reporting well over 95% success rates with minimal risk of serious complications. As with all medical procedures, the results are related to the experience and volume of the physician and center. The risk of recurrent AVNRT is less than 1% for patients with typical slow-fast AVNRT after ablation. The risk of recurrence is higher in patients with atypical forms of AVNRT, though the risk of complications is no different.
Complications of Slow AV Nodal Pathway Ablation
The complications of diagnostic electrophysiologic testing include bleeding at the site of venous access, pneumothorax (in the case of subclavian vein puncture), deep venous thrombosis, pericardial effusion or tamponade, and respiratory compromise from intravenous sedation. The primary complication related to ablation of the slow AV nodal pathway is that of inadvertent AV block. This complication occurs in less than 1% of cases and is almost always associated with a narrow QRS complex escape junctional rhythm. Factors that predispose to AV block include congenital heart disease (in which the AV conduction can be inferiorly displaced), an usual orientation of the coronary sinus ostium, or a prolonged refractory period of the fast pathway at baseline.
