Sinus Node and Atrio-ventricular Junction Modification/Ablation
Introduction
Inappropriate sinus tachycardia (IAST) is an uncommon entity that can cause debilitating symptoms and even a tachycardia-mediated cardiomyopathy.1,2,3 Generally, it is a diagnosis of exclusion following negative evaluation for secondary causes. Proposed mechanisms include 1) increased automaticity from an intrinsic defect in the sino-atrial node (SAN) and/or 2) sympathovagal imbalance.2 Catheter modification of the SAN provides an option for symptomatic, drug-refractory IAST.
The atrio-ventricular (AV) node provides electrical continuity between the atrium and ventricle and serves as a filter to prevent rapid ventricular rates during atrial fibrillation. However, short AV nodal functional refractory periods can result in rapid ventricular rates that might necessitate modification or ablation followed by permanent pacemaker implantation to achieve rate control.4,5,6,7
The purpose of this chapter is to:
Describe the anatomy of the sinus and AV node-His bundle axis.
Discuss the technique of sinus node modification.
Discuss different approaches of AV node modification/ablation.
SINO-ATRIAL NODE AND AV NODE-HIS BUNDLE AXIS
The SAN is a crescent-shaped epicardial structure (mean length = 13.5 mm) situated along the superolateral right atrium (RA) near its junction with the superior vena cava (SVC) and with its long axis running parallel along the sulcus terminalis (terminal groove).8 Because sinus nodal cells located cranially discharge at faster rates than caudal cells, the superior SAN is the initial target site for ablation during sinus node modification.
The compact AV node is a subendocardial structure located along the right interatrial septum posterior and inferior to the His bundle. The His bundle lies at the apex of the triangle of Koch, which is defined by the 1) ostium of the coronary sinus, 2) septal leaflet of the tricuspid valve, and 3) tendon of Todaro. The His bundle penetrates the crest of the interventricular septum where it can be recorded on both sides of the interventricular septum providing right- and left-sided approaches to AV junction ablation.
SINO-ATRIAL NODE MODIFICATION
The initial target site during SAN modification is the superior SAN identified by mapping the earliest site of atrial activation during sinus tachycardia (Figs. 16-1 and 16-2).9,10,11,12,13 Delivery of radiofrequency (RF) energy can cause initial acceleration of sinus tachycardia. Because of the close proximity between the right phrenic nerve and SAN, it is important to test for phrenic nerve capture by high-output pacing in order to avoid diaphragm paralysis during ablation. In the presence of diaphragmatic capture, the phrenic nerve can be monitored during RF delivery by pacing the right phrenic nerve with a catheter placed in the right subclavian vein (as done during right-sided pulmonary vein cryoablation). With ablation of the superior SAN, the earliest site of atrial activation shifts caudally along the SAN, resulting both in a reduction in sinus rate and P-wave amplitude in the inferior leads. Ablation lesions are progressively delivered caudally along the sinus node until the sinus rate is 1) reduced by 25% or below 90 bpm (baseline), 2) reduced 25%
or below 120 bpm (isoproterenol), and 3) accompanied by flattening of the inferior P-wave amplitude indicating a caudal shift in the SAN focus.10,11,13,14 Ablation can be facilitated by intracardiac echocardiography targeting the superior crista terminalis (the internal counterpart of the sulcus terminalis) and irrigated ablation catheters (because of the epicardial location of the SAN and the thick terminal crest separating the SAN from the endocardial cavity).8,14,15 In difficult cases, success might be achieved by targeting the arcuate ridge (band of myocardium connecting the superior crista terminalis to the septum near the superior limbus) or an epicardial approach.16,17
or below 120 bpm (isoproterenol), and 3) accompanied by flattening of the inferior P-wave amplitude indicating a caudal shift in the SAN focus.10,11,13,14 Ablation can be facilitated by intracardiac echocardiography targeting the superior crista terminalis (the internal counterpart of the sulcus terminalis) and irrigated ablation catheters (because of the epicardial location of the SAN and the thick terminal crest separating the SAN from the endocardial cavity).8,14,15 In difficult cases, success might be achieved by targeting the arcuate ridge (band of myocardium connecting the superior crista terminalis to the septum near the superior limbus) or an epicardial approach.16,17
FIGURE 16-2 SAN modification (transplanted heart). During donor IAST, the earliest site of atrial activation was along the anterolateral RA near the cavo-atrial junction (red). RF energy was delivered cranio-caudally along the SAN causing transient sinus arrest and a junctional escape rhythm. Note the slower recipient sinus rate (arrows) that persists unperturbed and fails to conduct to the ventricle (recipient-donor suture line) giving the appearance of AV block.
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