Mahmoud Houmsse, MD, and Anish Amin, MD
A 31-year-old woman with a 10-year history of palpitations is referred for an electrophysiologic (EP) study and consideration for radiofrequency ablation (RFA) for recurrent symptomatic paroxysmal supraventricular tachycardia (PSVT). Her symptoms start suddenly and are associated with chest pain and shortness of breath. The index episode terminated suddenly before she arrived at the emergency department (ED). Her initial evaluation, including 12-lead electrocardiogram (ECG), thyroid function testing, and echocardiogram was not revealing. Empiric medical therapy with atenolol initially suppressed her PSVT; however, breakthrough episodes have occurred over the past few months. Her most recent episode was recorded on an ECG as a narrow QRS complex tachycardia without an obvious P wave compared to baseline ECG (Figure 7-1A and B). Valsalva maneuver did not affect the tachycardia, and intravenous adenosine was administered, which successfully terminated her arrhythmia. Therapeutic options, including changing medical therapy versus EP study and RFA of her PSVT, were discussed with her. She requested the latter option since her symptoms were not controlled on medical therapy. Her EP study demonstrated dual AV node physiology and easily inducible typical atrioventricular nodal reentrant tachycardia (AVNRT). Slow pathway mapping and ablation was performed successfully, and postablation she had no inducible tachycardia or evidence of slow pathway function. Her atenolol was discontinued, and she has had no further episodes of tachycardia after long-term follow-up.
FIGURES 7-1A AND 7-1B Twelve-lead ECG during typical AVNRT and normal sinus rhythm. During typical AVNRT, the QRS complex is usually narrow, and the P wave is often absent due to simultaneous activation of the atrium and ventricle. If, however, the atrial depolarization is slightly delayed, a portion of the P wave may be seen at the end of the QRS complex and be manifest as a pseudo R’ wave in lead V1 or a pseudo S wave in the inferior leads. Figure 7-1A was taken during tachycardia at a rate of 173 bpm. No clear P wave was discernible, but terminal deflections were seen in leads V1 and II consistent with pseudo R’ and pseudo S waves (labeled R’ and S, respectively). A comparison to the baseline ECG (shown in Figure 7-1B) is required to confirm this, and as can be seen there were no R’ or S waves in leads V1 or II during normal sinus rhythm.
AVNRT is the most common type of regular narrow QRS complex SVT and accounts for approximately 60% to 70% of cases. There is a higher incidence in women and younger individuals, with the mean age of symptom onset at 30 years.1,2 The slow-fast variant of AVNRT accounts for nearly 90% of all AVNRT and is therefore referred to as typical AVNRT.
The onset of symptoms with AVNRT are usually paroxysmal in nature occurring suddenly without warning, but in some patients episodes can be brought on during high adrenergic states such as exercise. Symptoms that occur during AVNRT, like other forms of PSVT, are nonspecific and include palpitations, shortness of breath, chest pain, and dizziness. Frank syncope occurs rarely and appears to be rate-related since it is uncommon at rates less than 170 bpm.3
AVNRT utilizes both AV nodal and peri-AV nodal tissue as substrate for the reentrant circuit.2 This circuit is located within the triangle of Koch, which is boarded by the tricuspid annulus anteriorly, the tendon of Todoro posteriorly, and the coronary sinus inferiorly (Figure 7-2A and B). The triangle of Koch is divided into three zones: anterior, middle, and posterior. The anterior zone is located at the apex of the triangle and contains the compact AV node and initial portion of the His bundle. The middle zone is located just inferior to the anterior zone, and the posterior zone is located at the base of the triangle and contains the ostium of the coronary sinus. The fast and slow pathways that make up the reentrant circuit for typical AVNRT are also located within the triangle of Koch. The fast pathway is located in the anterior portion of the triangle in close proximity to the compact AV node. The slow pathway is found in the middle or posterior portions of the triangle often around the coronary sinus ostium. The fast and slow pathways join at the lower and upper common pathways. The latter is located within the AV node proximal to the bundle of His.4 Understanding this anatomy is especially important when ablative therapy is contemplated. Energy delivery in the anterior zone targeting the fast pathway carries a significant risk of creating AV block since this is where the compact AV node and proximal His bundle are located.
FIGURES 7-2A AND 7-2B Anatomy of the triangle of Koch. Figure 7-2A depicts the anatomy in the right anterior oblique (RAO) view, and Figure 7-2B depicts the anatomy in the left anterior oblique (LAO) view. The triangle of Koch is bordered anteriorly by the tricuspid valve annulus (TVA), posteriorly by the Tendon of Todaro (TT), and inferiorly by the coronary sinus ostium (CS os). The anterior (A) zone contains the compact atrioventricular node (AVN) and the fast pathway (FP). The middle (M) and posterior zones contain the slow pathway (SP), and the posterior zone also includes the coronary sinus ostium (CS os).
The basic components of a typical AVNRT circuit are a slow pathway that conducts in the antegrade direction, a fast pathway that conducts in the retrograde direction, and upper and lower common pathways which link the fast and slow pathways. Antegrade conduction over both a fast and slow AV nodal pathway (“dual AV nodal physiology”) can usually be demonstrated in patients with typical AVNRT. The fast pathway has more rapid conduction but usually has a longer refractory period compared to the slow pathway. When an appropriately timed premature atrial contraction occurs, it will block in the fast pathway and conduct over the slow pathway to the His bundle and ventricle resulting in significant prolongation of the AH and PR intervals compared to the normal sinus beat. This electrophysiologic (EP) phenomenon of changing conduction from the fast to the slow pathway is known as an “AV nodal Jump.”5 During an EP study, an AV nodal jump is defined as a 50 ms increase in the AH interval corresponding to a 10 ms decrease in the A1-A2coupling interval during atrial extrastimulus testing (Figure 7-3A and B).
FIGURES 7-3A AND 7-3B Dual AV nodal physiology. These figures demonstrate atrial extrastimulus pacing at a drive train of 550 ms. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), His bundle distal (His-d), His bundle proximal (His-p), and right ventricle apex (RVA). In Figure 7-3A, with an S2 coupling interval of 300 ms the corresponding atrial to His (AH) interval is 315 ms. In Figure 7-3B the S1S2coupling interval is 290 ms with a corresponding AH interval of 435 ms, an increase of 120 ms. An AH interval increase of >50 ms for a decrement in the S1S2coupling of 10 ms defines an AV nodal jump and indicates the presence of antegrade dual AV nodal physiology.
The finding of antegrade dual AV nodal physiology only defines the presence of antegrade fast and slow pathways, but it does not demonstrate the existence of a retrograde fast pathway, which is a necessary component of the AVNRT circuit. The presence of a retrograde fast pathway is suggested when there is rapid ventriculo-atrial (VA) conduction during ventricular pacing. Some patients with typical AVNRT may have very poor VA conduction or VA dissociation during baseline EP testing and may require the addition of an isoproterenol infusion to elicit fast pathway conduction.5 The presence of a retrograde fast pathway is confirmed if an AV nodal echo can be demonstrated during atrial pacing maneuvers (Figure 7-4). An AV nodal echo is the result of antegrade conduction down the slow pathway to the lower common pathway and then simultaneous conduction retrograde over the fast pathway to the atrium and antegrade over the His-Purkinje system to the ventricle. It is this simultaneous or “in parallel” conduction along with very rapid retrograde fast pathway conduction that results in the short VA times (≤70 ms recorded on the His bundle catheters) that are characteristic of typical AVNRT. In some cases the VA time during tachycardia may be zero or even negative. This can occur if the conduction time from the lower common pathway retrograde to the atrium is equal to or faster than the antegrade conduction time to the ventricle. If after an AV node echo the slow pathway is not refractory, then antegrade conduction can occur over the slow pathway, and typical AVNRT can be induced (Figure 7-5A and B).
FIGURE 7-4 AV nodal echo. This figure demonstrates atrial extrastimulus pacing at a drive train of 550 ms. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), His bundle (His), and right ventricle apex (RVA). An S1S2 coupling interval of 260 ms results in conduction down the slow pathway and a prolonged AH interval. At this degree of AH prolongation an atrial event (A) with a short VA conduction time occurs. This is an AV nodal echo and confirms the presence of retrograde fast pathway conduction.
FIGURE 7-5A Initiation of AVNRT. Figure 7-5A demonstrates atrial extrastimulus pacing at a drive train of 550 ms. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrial (HRA), His bundle distal (His-d), His bundle proximal (His-p), and right ventricular apex (RVA). An S1S2 coupling interval of 260 ms results in antegrade conduction down the slow pathway and initiation of typical AVNRT at a cycle length of 300 ms. The atrial, His, and ventricular electrograms are labeled A, H, and V, respectively, on the intracardiac recordings.
FIGURE 7-5B This figure demonstrates a spontaneous premature atrial contraction (PAC) initiating typical AVNRT. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), His bundle distal (His-d), His bundle proximal (His-p), and right ventricle apex (RVA). The atrial, ventricular, and His bundle electrograms are labeled A, V, and H, respectively, on the intracardiac recordings. The first two beats conduct over the fast pathway with an AH interval of 40 ms. The third atrial beat (A*) is a spontaneous premature atrial contraction, which blocks in the fast pathway and conducts over the slow pathway (SP = down arrows, AH = 240 ms). Subsequent retrograde conduction occurs over the fast pathway (up arrows), and tachycardia is initiated. The onset of the QRS is denoted as a solid line, and the earliest A is seen on the proximal His bundle recording. The VA time during tachycardia measured at proximal His bundle is 0 ms (solid line). The very short VA time during AVNRT is the result of simultaneous conduction from the lower common pathway retrograde to the atrium via the fast pathway and antegrade to ventricle via the His bundle (“conduction in parallel”) as well as rapid retrograde fast pathway conduction.
The AV relationship during sustained typical AVNRT is almost always 1:1; however, the atrium and ventricle are not obligatory components of the tachycardia circuit, and therefore AV or VA block can occur without termination of the arrhythmia.6 Infra-Hisian block below the lower common pathway is relatively common at the onset of AVNRT but usually extinguishes quickly as the bundle of His refractory period accommodates overtime. Block above the upper common pathway during AVNRT resulting in VA conduction block is far less common than AV block but has been reported.7
The clinical presentation and ECG findings of typical AVNRT, although suggestive of the diagnosis, are not specific for it, and therefore EP testing is needed to confirm the tachycardia mechanism.
Diagnostic Criteria for Typical AVNRT during EP Testing
Induction is dependent upon developing a critical degree of AH prolongation (Figure 7-5A and B).8
Induction is usually achieved by atrial burst or extrastimulus pacing but can occasionally be seen after ventricular overdrive pacing.
Septal VA interval ≤70 ms.
The earliest retrograde atrial activation is usually recorded near the compact AV node at the apex of the triangle of Koch on the His bundle recording catheter. In a small percentage (<10%) the earliest retrograde atrial activation may be recorded at the coronary sinus ostium or along the left side of the atrial septum.9
Atrial overdrive pacing at a rate slightly faster than the tachycardia should result in acceleration of the ventricular rate to the pacing rate with a long antegrade conduction time consistent with continued conduction down the slow pathway.
■ Upon termination of atrial pacing, if the tachycardia continues, the VA relationship on the first return tachycardia beat should be roughly the same as during stable tachycardia (“VA linking”).8
■ Antegrade block in the slow pathway terminates tachycardia.
Ventricular overdrive pacing from the right ventricle: Ventricular pacing entrainment is said to be present if pacing at a cycle length slightly shorter than the tachycardia cycle length (20 to 30 ms shorter) results in acceleration of the atrial rate to the pacing rate and upon termination the tachycardia continues.
■ Features of ventricular pacing entrainment of AVNRT (Figure 7-6)8
FIGURE 7-6 Entrainment of AVNRT during ventricular pacing. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), His bundle distal (His-d), His bundle mid (His-m), His bundle proximal (His-p), coronary sinus (CS) distal (1,2) to proximal (9,10), and right ventricle apex (RVA). The atrial, ventricular, and his bundle electrograms are labeled A, V, and H respectively on the intracardiac recordings. right ventricular pacing (S1) at a cycle length of 280 ms was performed during AVNRT, which had a cycle length of 310 ms. Ventricular pacing advanced the atrial electrogram to the ventricular pacing rate of 280 ms (1st arrow), and upon termination of pacing the tachycardia continued indicating that the tachycardia was entrained by pacing. The postpacing response was an AV response (2nd arrow), which rules out an atrial tachycardia as the mechanism. AV reentrant tachycardia was ruled out by the very short VA time (30 ms) measured at the CS ostium (CS 9,10), making typical AVNRT the correct diagnosis. The long postpacing interval (PPI)–tachycardia cycle length (TCL) difference of more than 115 ms (535 − 310 = 225 ms) and long stimulus to A interval (SA)–tachycardia VA interval difference of more than 85 ms (215 – 30 = 185 ms) after RV pacing entrainment are characteristic of AVNRT.8
■ An atrial-ventricular response postpacing
■ Postpacing interval (PPI)–Tachycardia cycle length (TCL) difference >115 ms
■ Stimulus to A interval (SA)–tachycardia VA interval >85 ms
Note: For ventricular pacing impulses to reach the AVNRT circuit they have to conduct retrograde through the His bundle to the AV node. Therefore, there must be complete capture of the ventricle without fusion prior to entrainment of AVNRT. Also, since the ventricle is not part of the reentrant circuit of typical AVNRT, VA dissociation during pacing does not rule out AVNRT as a possible mechanism.
The differential diagnosis for a very short septal VA time (<70 ms) tachycardia includes typical AVNRT, atrial tachycardia, and nonreentrant junctional tachycardia. An atrial tachycardia can usually be excluded by demonstrating an atrial-ventricular response after ventricular pacing entrainment. If ventricular pacing entrainment can’t be achieved, then atrial pacing maneuvers which demonstrate VA linking are useful to rule out atrial tachycardia as the mechanism. Although nonreentrant junctional tachycardia is a much less common arrhythmia, it can be quite difficult to differentiate from typical AVNRT since the VA timing relationships and response to ventricular overdrive pacing can be identical. A useful technique to help differentiate these arrhythmias has been described using PACs introduced during tachycardia. If a PAC introduced late into the tachycardia cycle length results in a short AV time (indicative of fast pathway conduction) and the tachycardia does not terminate, this rules out AVNRT as the mechanism. If a PAC introduced early in the tachycardia cycle length affects the subsequent ventricular timing with a long AV interval (suggestive of slow pathway conduction), this is highly suggestive of AVNRT as the mechanism.10
The aggressiveness of treatment for termination or prevention of AVNRT depends on the clinical scenario. The American College of Cardiology (ACC) and the American Heart Association (AHA) guidelines give an in-depth discussion of the management of patients with supraventricular arrhythmias, and the reader is directed there for a more comprehensive review.11
• Termination strategy
Hemodynamically unstable: Most patients with typical AVNRT are stable, but some patients may present with severe symptoms or hypotension, which require urgent restoration of sinus rhythm. This can be achieved by either an intravenous (IV) push of adenosine or direct current (DC) cardioversion.
■ Vagal maneuvers such as the Valsalva maneuver can be tried first.12
■ Adenosine is the next step if vagal maneuvers fail. Adenosine is >80% effective in terminating AVNRT.13 It should be used with caution or avoided in patients with severe bronchospastic lung disease.
■ IV nondihydropyridine calcium channel blockers (verapamil or diltiazem) or IV β-blockers are the second-line drug therapy. Potential side effects of these agents include hypotension and bradycardia.14
• Preventive strategy: Symptomatic and frequent AVNRT is usually treated with either long-term pharmacologic therapy or catheter-based ablative therapy. Patient preference as well as drug tolerance are the main factors in selecting either therapy.
Nondihydropyridine calcium channel blockers and β-blockers are first-line agents.
Class I and III antiarrhythmics can be effective but are usually avoided because of the increased risk of serious side effects (ie, proarrhythmia). These agents can be considered if calcium or β-blockers are not effective and ablation is not an option.
■ Catheter ablation is the therapy of choice for:
• Patients who fail or do not desire long-term medical therapy.
• Patients with highly symptomatic or poorly tolerated AVNRT.
The overall success rate for AVNRT ablation is high (>95%), and the recurrence rate after successful ablation is low (<5%). Ablation techniques targeting both the fast pathway and slow pathway have been described, but because of the much lower incidence of heart block (<1%) with the slow pathway approach, this has become the preferred technique. The slow pathway is targeted by positioning the tip of the ablation catheter in the middle or posterior zones of the triangle of Koch, often around the coronary sinus ostium. These regions are searched for locations with a fractionated atrial electrogram and A:V electrogram ratio of <1 (typically on the order of 1:3) (Figure 7-7). After an acceptable site is found, radiofrequency (RF) energy can be delivered in a titrated fashion, starting at a low power of 10 to 15 watts and progressively increasing the wattage to a target of 25 to 35 watts. During energy delivery, continuous monitoring of the rhythm for the emergence of a junctional rhythm and for any sign of AV block is of critical importance. The development of a relatively slow stable junctional rhythm with 1:1 VA conduction during RF delivery is the desired response (Figure 7-8). The occurrence of a junctional rhythm indicates that the ablation lesion is affecting tissue with a connection to the AV node. The presence of 1:1 VA conduction during the junctional rhythm is an indicator that fast pathway function is intact and that the patient will not have AV block after the ablation is terminated. If at any time during the ablation there is evidence of disruption of rapid VA conduction (VA block or a significant change in VA time), the application should be terminated immediately to minimize the risk of high grade AV block. The primary endpoint for ablation is to render the patient noninducible. In patients where reproducibility of tachycardia induction was not reliable, secondary endpoints such as elimination or modification of slow pathway function can be used. It is important to understand that it is not necessary to completely eliminate all slow pathway function and that the presence of a single AV node echo is an acceptable endpoint in most patients.
FIGURE 7-7 Slow pathway ablation target site. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), ablation proximal (ABL-p), ablation distal (ABL-d), and right ventricle apex (RVA). The atrial, ventricular, and electrograms are labeled A and V, respectively, on the intracardiac recordings. The ideal slow pathway site should have an A/V ratio <1 along with a fractionated atrial electrogram as seen on the ablation distal recording.
FIGURE 7-8 Junctional beats during slow pathway catheter ablation. Shown are surface leads I, II, and V1 and intracardiac recordings from the high right atrium (HRA), ablation proximal (ABL-p), ablation distal (ABL-d), and right ventricular apex (RVA). The atrial and ventricular electrograms are labeled A and V, respectively, on the intracardiac recordings. The first two beats are sinus beats (S), and on the third beat there is a change in the atrial activation sequence with the atrial electrogram on the AB p occurring before the atrial electrogram on the HRA, indicating the emergence of a junctional rhythm and the last three beats are clearly junctional (J). It should be noted that during the junctional rhythm there is consistent 1:1 conduction to the atrium with a short VA time indicating that fast pathway conduction is intact.
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