Atrioventricular (AV) nodal–dependent tachycardias comprise a specific subgroup of rapid, regular supraventricular arrhythmias that critically depend on conduction through the AV node for their perpetuation. The most common forms are AV nodal reentrant tachycardia (AVNRT) and AV reciprocating tachycardia (AVRT), the latter of which uses an accessory pathway (AP) as the retrograde limb of the circuit. The anatomic location around the mitral or tricuspid annulus of APs can be identified precisely at the time of electrophysiologic testing but can also be predicted based on the morphology of retrograde P waves during tachycardia or characteristic delta waves in those patients in whom these arrhythmias occur as a component of Wolff-Parkinson-White (WPW) syndrome. AV nodal–dependent tachycardias are typically initiated by premature atrial or ventricular complexes and have reasonably specific characteristics that allow their differentiation. Although both are short RP tachycardias, AVRT must have a ventriculoatrial (VA) or RP interval of at least 70 msec, whereas most AVNRTs have intervals of less than 60 msec, with retrograde P waves presenting as a pseudo-R wave in surface electrocardiogram (ECG) lead V₁ during tachycardia. In some patients with APs, a reverse-direction tachycardia with anterograde conduction through the AP may occur, producing a maximally preexcited QRS complex on the surface ECG. Some patients with WPW syndrome are at potential risk for atrial fibrillation (AF) degenerating into ventricular fibrillation (VF). APs with unusual conduction characteristics contribute to the occurrence of preexcitation variants, including the permanent form of junctional reciprocating tachycardia (PJRT) and atriofascicular reentry. Because of their dependence on AV nodal conduction for their maintenance, AV nodal–dependent arrhythmias may be acutely terminated by vagal maneuvers or administration of adenosine or verapamil. Wide-complex tachycardias in these patients must be carefully approached without using drugs that accelerate AP conduction, which can lead to VF. Both pharmacologic and nonpharmacologic therapies may be applied in the long term for managing patients with these arrhythmias. Drug therapy may be directed at the AV node, the AP, or the initiating atrial or ventricular extrastimuli. Ablative therapy has also emerged as the mainstay of nonpharmacologic treatment of these arrhythmias.

AV nodal–dependent tachycardias comprise a specific subgroup of rapid, regular supraventricular arrhythmias that critically depend on conduction through the AV node for their perpetuation. These arrhythmias typically use the normal AV conduction system as the anterograde limb of the reentrant circuit and therefore present with a narrow QRS complex on the surface ECG, as shown in Figure 65.1. Unlike atrial flutter or atrial tachycardias, which may continue despite the presence of high-grade AV block, AV nodal–dependent tachycardias are typically
terminated by vagal, drug, or nonpharmacologic interruption of AV nodal conduction.

The most common of the AV nodal–dependent arrhythmias are AV nodal reentrant tachycardia (AVNRT) and AV reciprocating tachycardia (AVRT). AVNRT involves anterograde and retrograde components of the reentrant substrate that are near or within the compact portion of the AV node and neighboring bundle of His. AVRT involves the AV node and an AP as the limbs of the tachycardia circuit (Fig. 65.2).

These arrhythmias have been a focus of extensive clinical interest during the last 100 years and have prompted numerous studies to clarify the underlying electrophysiology. Kent provided an early description of what we now refer to as the normal AV conduction system (1). Mines provided the first description of reentry in the AV node in 1913, and his explanation of the possible physiologic mechanism of this arrhythmia is essentially what we now refer to as “dual AV nodal physiology” (2). In addition, Kent (3) identified anomalous muscular bundles connecting the atria and ventricles. Building on Kent’s observations, Mines (4) suggested that such a pathway may serve as a component of a possible reentrant circuit.

By the end of the first decade of this period, a variety of case reports documented the occurrence of relatively benign, rapid, regular tachycardias accompanied by palpitations (5,6,7,8). Wood et al. (7) reported a patient with a short PR interval and prolonged QRS complex who died during an attack of paroxysmal tachycardia. Serial histological sections of a portion of this patient’s AV groove showed three muscular connections between the right auricle and ventricle at the right lateral border of the heart. Wolferth et al. (5) hypothesized that such accessory connections capable of AV conduction may be responsible for both ventricular preexcitation during sinus rhythm and the paroxysms of tachycardia in these patients.

In 1930 the combination of paroxysmal tachycardias of this type along with a bundle-branch-block QRS morphology and a short PR interval were codified as the Wolff-Parkinson-White (WPW) syndrome (8). The existence of apparent dual AV nodal physiology as additional avenues of AV conduction was further suggested by others (9,10,11), and in 1963 Kistin postulated the existence of multiple AV nodal pathways in humans (12). Other investigators also subsequently described the possibility of triple or multiple AV nodal pathways (13,14,15,16,17).

The understanding of the rhythm disorders created by these connections took a giant leap forward with the advent of catheter-based electrophysiologic studies (18,19,20,21,22,23). By positioning multiple recording electrodes within the heart and using electrical stimulation techniques, it has been possible to elucidate the roles of the AV node and AP in supraventricular tachycardias (SVTs). Furthermore, this information has also expanded our understanding of macroreentrant arrhythmias in general. In this regard, the AV nodal–dependent SVTs with their discrete anatomic components can be viewed as the “schoolmaster” of reentrant arrhythmias. Since then, volumes have been written about the preexcitation syndromes, their accompanying SVTs, and AVNRTs (24,25,26,27). More recently, the introduction of more advanced computerized and optical mapping techniques with improved resolution has allowed more precise elucidation of arrhythmia substrates and mechanisms (28,29,30).

These tachycardias also provided the substrate for the first foray into nonpharmacologic therapy for arrhythmias. In the late 1960s, several institutions (31,32) attempted to interrupt APs as a definitive cure for SVT. The first successful division of such a pathway by Sealy (32,33) in 1968 permanently cured a North Carolina man of his recurrent palpitations, firmly established the reentrant nature of AP-dependent arrhythmias, and ushered in the era of nonpharmacologic management of cardiac arrhythmias. Since then, several thousand APs have been surgically interrupted (34,35,36,37,38,39).

Based on lessons learned from such surgical interruption of APs, drug therapy for these arrhythmias has been largely supplanted by development of closed-chest, catheter-based ablation of these reentrant circuits. Radiofrequency (RF) ablation was originally reported for APs in 1987 (40) and for the slow pathway for cure of AVNRT in 1992 (41). RF ablation has been further refined by a number of investigators (42,43,44,45,46,47,48) and applied to tens of thousands of patients with AVRT and other AV nodal–dependent tachycardias. In addition to RF, other energy sources for catheter ablation have been developed, such as cryothermy, laser, ultrasound, and microwave sources (49). For AV nodal–dependent tachycardias, the most extensive experience has been with cryothermy (50,51), and there has been limited experience with lasers (52). Other energy sources for catheter ablation, such as ultrasound and microwaves, have not yet been studied extensively for AV nodal–dependent
tachycardias. Because of the high success rates and low accompanying risk, catheter ablation has nearly replaced drug therapy as the mainstay of treatment for AV nodal–dependent arrhythmias. Each of these historic milestones marks important progress in both our understanding of these arrhythmias and the development of effective clinical management strategies.