Preexcitation, Atrioventricular Reentry, Variants

Classification of Accessory Pathways

The most common variety of AP is a periannular AV connection. These pathways consist of atrial tissue that “short circuit” the AV groove and insert into the base of the ventricle. They can bridge the AV groove anywhere along the tricuspid or mitral annulus but rarely occur in the region of the aortomitral continuity. AV pathways can conduct bidirectionally, retrogradely only, or, less commonly, anterogradely only. Over time, patients may spontaneously lose anterograde or retrograde AP conduction, or both. Given that these pathways are composed of atrial tissue, they differ from AV nodal tissue in that they typically exhibit little or no slowing of conduction with rapid input rates.

Other variants of APs include (1) atriofascicular pathways, connecting the right atrium to the distal right bundle branch (RBB) system; (2) fasciculoventricular pathways, connecting the His bundle to the summit of the ventricle; (3) nodofascicular/nodoventricular pathways, connecting the AV node to the distal RBB or right ventricle (RV), respectively; and (4) appendage-ventricular connections.

Electrocardiogram Features of Accessory Pathways

Anterograde conduction over an AP results in an ECG pattern of preexcitation, which involves a short PR interval and widened QRS complex with initial slurring known as a delta wave. This preexcitation pattern is generated by fusion of ventricular activation via both the AV node/His-Purkinje system and the AP. Premature atrial complexes or any other perturbation that slows AV nodal conduction accentuates preexcitation because, unlike the AV node, the AP typically does not have decremental conduction properties. Anything that accelerates conduction through the AV node (e.g., exercise or atropine) will decrease the degree of preexcitation. Likewise, the degree of preexcitation is accentuated if an ectopic atrial impulse arises closer to the atrial insertion of the AP, and preexcitation disappears totally during a junctional rhythm. Preexcitation may be intermittent, implying a long anterograde AP refractory period. APs that conduct anterogradely and thus generate a delta wave are termed manifest pathways , and those that conduct retrogradely only and do not generate delta waves are termed concealed APs; the latter can participate in orthodromic reciprocating tachycardia (RT) but do not allow for preexcited tachycardias. Some anterogradely conducting APs, especially left lateral APs distant from the AV node, may show little or no preexcitation until AV node conduction is slowed (e.g., with adenosine), or an atrial extrasystole arises close to the origin of the AP, allowing for the appearance of the delta wave. It is important to distinguish these patients from those with true concealed APs because atrial fibrillation (AF) with a rapid ventricular response would still be a risk in the former.

The orientation of the delta wave (first 0.4 seconds of the QRS) during sinus rhythm helps localize the AP. Several detailed algorithms have been developed to localize APs. Put simply, however, delta waves that are positive in lead V ₁ suggest left-sided AP locations, and delta waves predominantly negative in V ₁ suggest right-sided APs. Positive delta waves in leads II, III, and aVF suggest anterosuperior locations; those negative in II, III, and aVF suggest posteroinferior locations along the AV annulus. Nevertheless, accuracy of AP localization from the surface ECG is limited because of (1) difficulty determining the delta wave vector because of QRS fusion, (2) varying cardiac orientation and rotation within the chest cavity, (3) the fact that some important location distinctions are only a few centimeters apart (e.g., right anterior free wall and right superoparaseptal [anteroseptal] APs), (4) slight variations in chest and limb lead placement, and (5) fusion of delta waves if there is more than one AP.

Arrhythmias Associated with Accessory Pathways

Tachycardias associated with APs can be classified as either orthodromic RT or preexcited tachycardias. Orthodromic RT is the most common arrhythmia in patients with APs and involves anterograde conduction via the normal AV node/His-Purkinje system and retrograde conduction via the AP; this results in a regular narrow QRS tachycardia (i.e., without delta waves) or, if bundle branch block (BBB) aberrancy occurs, a wide QRS tachycardia with a left bundle branch block (LBBB) or right bundle branch block (RBBB) pattern.

Preexcited tachycardias are those with anterograde ventricular activation via the AP. Preexcited tachycardias are characterized by a wide, bizarre QRS complex originating from the base of the heart (positive V ₅ –V ₆ ), oriented in the same direction as the delta wave, and not resembling the typical RBBB or LBBB morphology. Mechanisms of preexcited tachycardias include (1) antidromic RT (the AP is an integral part of the tachycardia circuit with anterograde conduction via the AP and retrograde conduction via the AV node/His-Purkinje system or, less commonly, a second AP) or (2) tachycardias in which the AP is a bystander (e.g., atrial tachycardia, atrial flutter, AF, or AV node reentry with preexcitation because of anterograde AP conduction). Preexcited AF is characterized by very rapid and irregular rates with various degrees of QRS fusion.

Rarely, one AP is used for anterograde conduction during tachycardia and a second AP is used for retrograde conduction. Because the natural AV nodal delay is not incorporated in such a tachycardia circuit, the circuit must include substantial atrial and ventricular tissue to allow tachycardia to perpetuate; therefore the two APs must be located in disparate regions of the heart.

A special case of antidromic reciprocating tachycardia, using an atriofascicular pathway for anterograde conduction and the His-Purkinje/AV nodal conduction system for retrograde conduction, is considered later.

Clinical Features of Atrioventricular Reentrant Tachycardia

Typical atrioventricular reentrant tachycardia (AVRT) patients have a long history of intermittent palpitations, presenting when relatively young compared with patients with supraventricular tachycardias associated with structural heart disease such as AF. Symptoms range from very mild, short-lived episodes of palpitations that terminate spontaneously or with vagal maneuvers to episodes that are prolonged and associated with shortness of breath, chest discomfort, and near syncope. Older patients may experience exacerbation of angina by episodes of tachycardia. An occasional patient experiences hemodynamic collapse from AVRT, although when this occurs, the coexistence of AF with rapid anterograde conduction over an AP should be excluded. The patient can often state that the tachycardia starts and terminates suddenly and can sense that it is regular. Some patients may have noted that maneuvers such as holding their breath or bending over (Valsalva-like maneuvers) suddenly terminate the palpitations.

Electrocardiographic Features of Atrioventricular Reentrant Tachycardia

The sinus rhythm ECG may demonstrate a delta wave or may be normal. Twelve-lead ECG obtained during orthodromic AVRT usually shows a regular narrow QRS tachycardia, although either functional LBBB or RBBB may occur. Tachycardia initiation and termination are sudden. Termination may occur either spontaneously or after administration of an AV nodal blocking drug such as adenosine (tachycardia terminates with a P wave not followed by a QRS complex). On the surface ECG, the P wave is usually located within the ST-T segment (RP < PR interval). In some cases, the P wave may be difficult to identify, especially if functional BBB is present. If the P wave is located within or just after the inscription of the QRS complex, AV nodal reentrant tachycardia is likely and AVRT is excluded; if the P wave is in the ST-T segment, the likely diagnosis is AVRT, but slow/slow AV nodal reentrant tachycardia cannot be excluded. A negative P wave in lead 1 during tachycardia suggests a left atrial insertion site of the AP (but does not exclude a left atrial tachycardia). AV block may occur during atrial tachycardia or AV nodal reentry, but it cannot occur during AVRT without terminating the tachycardia because the ventricles are part of the tachycardia circuit. Likewise, slowing of tachycardia rate and an increase in the ventriculoatrial (VA) interval because of functional BBB ipsilateral to the AP is unique for AV reentry because AVRT is the only form of supraventricular tachycardia in which ventricular structures participate in the reentrant circuit.

Antidromic AVRT is a regular wide QRS tachycardia. The QRS morphology is not typical of either LBBB or RBBB aberration but is identical to the QRS during total preexcitation. Antidromic tachycardias are difficult to distinguish electrocardiographically from ventricular tachycardia. Because of the wide QRS complexes, P waves are difficult to identify. There should be no evidence of VA dissociation (e.g., fusion or capture complexes) and no evidence of AV block during tachycardia. There is usually a manifest delta wave on the surface ECG once the tachycardia has been terminated.

The differential diagnosis of supraventricular tachycardias in which the RP interval is greater than the PR interval should be mentioned. If the P waves are negative in the inferior leads, atrial tachycardia or an atypical variety of AV nodal reentry (retrograde conduction via a slow AV nodal pathway and anterograde conduction via a fast AV nodal pathway) are possible. In addition, some AVRTs using slowly conducting APs for the retrograde limb have long VA conduction times and consequently very long RP intervals. This may occur in patients with Ebstein anomaly and is classic in an entity known as the permanent form of junctional reciprocating tachycardia (PJRT), using a concealed AP with slow retrograde conduction properties during orthodromic RT (see later).

Electrophysiology Studies in Patients with Accessory Pathways and Ventricular Preexcitation

Periannular APs are composed of atrial muscle and therefore typically (but not universally) demonstrate little decrement in conduction time with rapid pacing and premature stimulation. Likewise, they usually do not slow or block with adenosine, although important exceptions exist. They typically cross the AV annuli obliquely, which is an important consideration for mapping and ablation.

Atrial pacing at progressively shorter cycle lengths or prematurity enhances ventricular preexcitation by prolonging AV nodal conduction: The A-H interval prolongs but the stimulus-to-delta interval is usually unchanged, resulting in shortening of the HV interval. Pacing at sites closer to the AP enhances preexcitation for any given pacing cycle length (CL); the shorter the stimulus-to-delta interval, the closer that pacing site is to the AP atrial insertion.

Electrophysiologic Features of Orthodromic Atrioventricular Reentrant Tachycardia

AVRT must be differentiated from atrial tachycardias and from AV nodal reentrant tachycardias (see Chapter 70 ). All of these tachycardias may be inducible with either atrial or ventricular pacing techniques. Circumstantial evidence that favors AVRT would be the presence of a delta wave during sinus rhythm. The demonstration of dual AV nodal physiology may suggest AV nodal reentrant tachycardia, but dual AV nodal physiology may also be found in patients with APs. During electrophysiologic (EP) study, orthodromic AVRT is usually a narrow QRS tachycardia with each ventricular deflection preceded by a His bundle deflection and a normal HV interval. If a fixed or functional BBB is present during tachycardia, each QRS complex is still preceded by a His deflection with a normal or prolonged HV interval. There must be one atrial electrogram associated with each ventricular electrogram because the atrium is a necessary part of the tachycardia circuit, and AV block cannot occur with perpetuation of the tachycardia. The VA intervals, representing retrograde AP conduction, are usually constant (unless two retrogradely conducting accessory pathways are present). Conduction characteristics of the atrium, His-Purkinje system, ventricle, and accessory pathway are usually relatively constant; thus tachycardia CL variations in the same patient are predominantly because of the effect of changes in autonomic tone on AV nodal conduction. CL alternans during AVRT is common, with the site of alternation being within the AV node (atrial-His [AH] alternans). Adenosine administration during AVRT terminates the tachycardia suddenly by anterograde AV nodal block (atrial activation without subsequent ventricular activation).

Induction of Atrioventricular Reentrant Tachycardia

Orthodromic AVRT can be induced by either atrial or ventricular premature stimuli ( Fig. 74.1 ). If induced by an atrial extrastimulus, the impulse must (1) block anterogradely in the AP and (2) travel across the AV node/His-Purkinje system with sufficient delay so that the AP and surrounding atrium have recovered excitability when the impulse arrives retrogradely. After the atrial echo, the AV node/His-Purkinje system must be sufficiently excitable to conduct anterogradely again to produce ventricular activation and subsequently a sustained tachycardia. Autonomic manipulation with atropine or isoproterenol is necessary in some patients to produce a sustained tachycardia.

Induction of orthodromic AVRT using premature ventricular stimuli requires that the impulse block retrogradely in the His-Purkinje system (almost always before reaching the AV node) and travel over the accessory pathway to the atrium. The AV node will thus be excitable anterogradely and provide enough delay so that the His-Purkinje system may recover.

Ventriculoatrial Intervals During Atrioventricular Reentrant Tachycardia

Because the impulse during AVRT must propagate through the ventricle before reaching the AP, a finite VA interval is mandatory in AVRT (in contrast to AV nodal reentry in which atrial and ventricular activation may be simultaneous). The shortest VA interval in AVRT must be greater than 60 ms. Values less than these exclude AVRT, although values greater than these do not exclude (but are unusual in) AV nodal reentry. In the case of septal APs, the VA interval during RV pacing approximates that during AVRT; if the AP is left free wall, the VA interval during RV pacing is longer than that during AVRT because of transseptal conduction. The VA interval during RV pacing in patients with AV nodal reentry is usually much longer than that during tachycardia; the VA interval during AV nodal reentry does not represent a true conduction interval but instead represents the relative anterograde and retrograde conduction times from the site of reentry within the AV node.