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 .
- 1.
Sinus tachycardia
- 2.
Atrial tachycardia
- 3.
Atypical atrioventricular nodal reentrant tachycardia
- 4.
Atrioventricular reentrant tachycardia caused by slowly conducting concealed accessory pathways
- 5.
Nonparoxysmal junctional tachycardia with 1:1 retrograde conduction
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 ).
Electrophysiologic classification
The recognition of the fact that AVNRT may present with atypical retrograde atrial activation has made diagnosis of the arrhythmia as well as classification attempts more complicated. Heterogeneity of both fast and slow conduction patterns has been well described, and all forms of AVNRT may display anterior, posterior, and middle or even left atrial retrograde activation patterns.
Typical AVNRT
In the slow–fast form of AVNRT the onset of atrial activation appears before, at the onset, or just after the QRS complex, thus maintaining an atrial-His/His-atrial ratio AH/HA greater than 1 ( Fig. 14.4 ).
The VA interval measured from the onset of ventricular activation on surface electrocardiogram (ECG) to the earliest deflection of the atrial activation in the His bundle electrogram is 60 or less. Although typically the earliest retrograde atrial activation is recorded at the His bundle electrogram, detailed mapping studies have demonstrated that posterior or even left septal fast pathways may occur in up to 7.6% in patients with typical AVNRT ( Figs. 14.5–14.7 ).
Atypical AVNRT
Atypical AVNRT is seen in approximately 6% of all AVNRT cases, and in some patients may coexist with the typical form. A higher incidence of atypical AVNRT has been documented in athletes. In the so-called fast–slow form of AVNRT, retrograde atrial electrograms begin well after ventricular activation with an AH/HA ratio less than 1, indicating that retrograde conduction is slower than antegrade conduction. The AH interval is less than 185 to 200 ms. The VA interval measured from the onset of ventricular activation on surface ECG to the earliest deflection of the atrial activation in the His bundle electrogram is more than 60 ms. Earliest retrograde atrial activation generally is at the base of the triangle of Koch, near the coronary sinus ostium, but can be variable, with eccentric atrial activation at the lower septum or even the distal coronary sinus ( Figs. 14.8 and 14.9 ).
In the slow–slow form, the AH/HA ratio is greater than 1 and the AH interval greater than 200 ms, but the VA interval is greater than 60 ms, suggesting that two different slow pathways are used for both anterograde and retrograde activation. Earliest retrograde atrial activation is usually at the coronary sinus ostium, but variants of left-sided atrial retrograde activation have also been published. , The distinction between fast–slow and slow–slow forms is of no practical significance, and certain cases of atypical AVNRT cannot be classified according to described criteria ( Fig. 14.10 ).
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