Atrioventricular junctional tachycardias

Atrioventricular nodal reentrant tachycardia

Definition

Atrioventricular nodal reentrant tachycardia (AVNRT) denotes reentry in the area of the atrioventricular (AV) node. Several models have been proposed to explain the mechanism of the arrhythmia in the context of the complex anatomy of the AV node and its atrial extension, but its exact circuit remains elusive.

Pathophysiology

The concept of dual AV nodal pathways as the substrate for AVNRT dates from 1956 when Moe et al. demonstrated evidence of a dual AV conduction system in dogs. It was postulated that a dual conduction system was present, one having a faster conduction time and longer refractory period (fast pathway), the other having a slower conduction time and shorter refractory period (slow pathway). At a critical coupling interval the premature impulse blocks in the faster pathway and conducts in the still excitable slow pathway, causing a sudden jump in the AV conduction time. After that, the impulse returns to the atria via the fast pathway, and an AV nodal echo beat or sustained tachycardia results ( Fig. 14.1 ). Denes et al. in 1973 ascribed episodes of paroxysmal supraventricular tachycardia to AV node reentry as a result of the presence of dual atrioventricular nodal pathways and, using His bundle recordings and the atrial extrastimulus method, demonstrated sudden prolongation of the AH interval in a patient with dual atrioventricular nodal pathways (so-called atrioventricular conduction jump). In approximately 6% of patients with AV nodal reentry, and at a higher rate in athletes, retrograde conduction is thought to proceed over the slow pathway and may result in an atypical form of AVNRT ( Fig. 14.2 ). In these patients, antegrade conduction curves are not always discontinuous. This pattern of conduction and a potentially incessant nature can also be caused by concealed septal accessory pathways with decremental properties.

The concept of longitudinally dissociated dual AV nodal pathways that conduct around a central obstacle with proximal and distal connections can provide explanations for many aspects of the electrophysiologic behavior of these tachycardias, but several obscure points remain. These pathways have not been demonstrated histologically, the exact circuit responsible for the reentrant tachycardia is unknown, and critical questions still remain unanswered. There has been considerable evidence that the right and left inferior extensions of the human AV node may provide the anatomic substrate of the “slow” pathway, whereas inputs to the node especially from the atrial septum may act as the “fast” pathway. ^, Variable gap junction connectivity due to differential expression of connexin isoforms in the area of the AV nodal extensions, variability in the arrangement of the superficial atrial muscle fibers in the area of the triangle of Koch, and, perhaps, involvement in the circuit of remnants of the primary ring, described as “ring tissues”, may also play a role. A probabilistic model of the tachycardia circuit for all forms of atrioventricular nodal reentrant tachycardia based on the concept of atrionodal inputs and connexin expression has been proposed ( Fig. 14.3 ).

There is evidence that spontaneous AVNRT can be the first clinical manifestation of concealed Brugada syndrome, and it has been postulated that genetic variants that reduce the sodium current (I _Na ) may predispose to expression of both phenotypes.

Diagnosis

Typically AVNRT is a narrow-complex tachycardia (i.e., QRS duration < 120 ms) unless there is aberrant conduction, which is usually of the right bundle branch block (RBBB) type, or a previous conduction defect exists. Tachycardia-related ST depression and RR interval variation may be seen. QRS alternans may be seen but is more common in atrioventricular reentrant tachycardia (AVRT).

In the typical form of AVNRT (also called slow-fast AVNRT), abnormal (retrograde) P′ waves are constantly related to the QRS and in the majority of cases are indiscernible or very close to the QRS complex. Thus P′ waves are either masked by the QRS complex or seen as a small terminal P′ wave (a pseudo-R′) that is not present during sinus rhythm (see Fig. 14.1 ).

In the atypical form of AVNRT, P′ waves are clearly visible before the QRS (i.e., RP′ > P′R), denoting a “long-RP tachycardia,” and are negative or shallow in leads II, III, aVF, and V ₆ but positive in V ₁ (see Fig. 14.2 ). Other causes of long-RP tachycardia are presented in Box 14.1 .

Although AV dissociation or ventriculoatrial (VA) block is usually not seen, it can occur because neither the atria nor the ventricles are necessary for the reentry circuit. If the tachycardia is initiated by atrial ectopic beats, the initial (ectopic) P′ wave usually differs from the subsequent (retrograde) P′ waves (see Fig. 14.1 ).