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Logo of thijTexas Heart Institute JournalSee also Cardiovascular Diseases Journal in PMCSubscribeSubmissionsTHI Journal Website
Tex Heart Inst J. 2009; 36(5): 477–479.
PMCID: PMC2763469

Sinus Arrest during Radiofrequency Ablation of the Atrioventricular-Node Slow Pathway

Implications and Possible Mechanisms


Radiofrequency ablation has been associated with changes in autonomic function. In this case, a 52-year-old woman was referred for electrophysiologic study of recurrent supraventricular tachycardia. Typical slow/fast atrioventricular node re-entry tachycardia was induced and confirmed during the study. Radiofrequency ablation of the slow pathway of the atrioventricular node led to sinus arrest, which resolved once ablation was stopped. Given the distance of the ablation site from the sinus node, we inferred that mechanisms other than direct injury to the sinus node were involved. To our knowledge, this is only the 2nd reported finding of sinus arrest during slow-pathway ablation of the atrioventricular node. This case highlights the complex interaction between the autonomic nervous system and the cardiac conduction system. Possible mechanisms include a Bezold-Jarisch reflex and modification of the intrinsic autonomic nervous system.

Key words: Afferent pathways, autonomic nervous system diseases, catheter ablation/adverse effects, electrophysiology, heart conduction system, parasympathetic nervous system, radiofrequency ablation, tachycardia, supraventricular/therapy

Radiofrequency ablation (RFA) is associated with changes in autonomic function.1 Because the autonomic nervous system of the heart comprises exceedingly complex neural networks, significant changes in autonomic function may occur at locations not in proximity to an ablation site.

Case Report

In February 2008, a 52-year-old woman who had a long-standing history of palpitations despite treatment with β-blockers was referred for an electrophysiologic study and possible ablation. A 12-lead electrocardiogram during tachycardia revealed a short R–P tachycardia with a ventricular rate of 180 beats/min (Fig. 1). The patient underwent an electrophysiologic study with catheters placed in the high right atrium, the coronary sinus, the region of the bundle of His, and the right ventricular apex. Baseline intervals were as follows: CL, 724 msec; AH, 87 msec; HV, 50 msec; PR, 171 msec; QRS, 90 msec; and QT, 374 msec. The electrophysiologic study induced clinical tachycardia characterized by an AH jump during atrial extrastimulus testing at 600/260 msec—consistent with dual-pathway atrioventricular (AV)-nodal physiology. In addition, the ventriculoatrial time during tachycardia was 40 msec with concentric retrograde activation. These findings confirmed our impression of typical slow/fast AV-node re-entry tachycardia.

figure 26FF1
Fig. 1 A 12-lead electrocardiogram shows clinical tachycardia.

We attempted radiofrequency ablation using a large-curve 4-mm Blazer® II HTD ablation catheter (Boston Scientific Corporation; Natick, Mass). Using fluoroscopic and electrographic guidance, we positioned the catheter anterior to the coronary sinus ostium, at the site of the slow pathway of the AV node. At the beginning of each RFA, the patient developed sinus arrest, which persisted for 2 to 3 seconds after RF was turned off (Fig. 2). This finding occurred in the absence of pain. This phenomenon occurred multiple times upon the initiation of RFA.

figure 26FF2
Fig. 2 Sinus arrest of 4.6 seconds' duration (length of arrow) caused by radiofrequency ablation (RFA). After each ablation attempt was stopped, sinus-node function returned after 2 to 3 seconds (after 2.6 seconds, in this particular RFA attempt). Beat-to-beat ...

Ultimately, we were able to perform successful RFA at this site, as manifested by junctional tachycardia indicative of slow-pathway modification. Postprocedure intervals were normal (CL, 677 msec; AH, 77 msec; HV, 41 msec; PR, 166 msec; QRS, 81 msec; and QT, 361 msec). The patient has been symptom free during 6 months of follow-up.


To our knowledge, this is only the 2nd report in the literature of sinus arrest during RFA of the slow pathway of the AV node.2 On the other hand, transient autonomic dysfunction during and after RFA has been described often.1 This includes sinus bradycardia during ablation, as well as inappropriate sinus tachycardia that may persist after ablation.1 In addition, sinus node dysfunction during ablation can occur at sites distant from the sinus node. The proposed mechanisms include direct neural connections, initiation of cardiac reflexes, or direct injury to autonomic fibers during ablation.1

Transient or permanent AV block is a well-described phenomenon during slow-pathway ablation. Additionally, late AV block has been reported in a small percentage of patients.3 Early AV block can be explained by direct injury to the adjacent fast pathway during ablation, by permanent scarring after ablation (leading to diminished AV-nodal function)—or by both.

The sinus node is not in proximity to the slow pathway of the AV node, yet the clear association in our patient between RFA and sinus arrest suggests neural connections between the 2 regions. The Bezold-Jarisch reflex is a possible mechanism: the inhibitory reflex from vagal afferent nerve fibers originating in the heart leads to an increase in parasympathetic tone and conversely to a decrease in sympathetic stimulation. Clinically, this results in bradycardia and hypotension.4,5 Although the original reports suggest that the afferent nerve fibers arise from the inferoposterior left ventricle, subsequent reports suggest evidence of afferent fibers throughout the heart.4 Histologic studies have noted that unmyelinated C fibers, which are believed to be involved in vasodepressor reflexes, are grouped predominantly in the posterior left ventricle, around the pulmonary veins, in the roof of the left atrium, and in the lateral wall of the right atrium.6 Two reports in the literature describe sinus arrest during RFA of left-sided accessory pathways7,8; both suggest Bezold-Jarisch phenomenon as the underlying mechanism. In addition, 1 case series describes a 15% incidence of significant sinus arrest, bradycardia, or both during isolation of the superior pulmonary veins for paroxysmal atrial fibrillation.9 Although not proved in our patient, ablation at the slow-pathway region may have activated afferent vagal fibers, which led to the sinus arrest.

Another plausible mechanism to explain the clinical findings is activation of the intrinsic cardiac ganglionated plexus in the region of the AV node. Previous literature has described the occurrence of a progressive AV-node Wenckebach period, as well as transient 3rd-degree AV block, during high-frequency stimulation of parasympathetic nerves adjacent to the proximal coronary sinus.10 The present case may be an instance of direct stimulation of a nearby ganglionated plexus during attempted ablation in the slow-pathway region.

Finally, direct injury to sensory fibers from radiofrequency ablation might have led to changes in autonomic tone and ultimately to sinus arrest. The transient nature of the sinus arrest—without persistence of arrest, without bradycardia after RFA, and with normal post-ablation sinus node function—suggests that direct injury to nerve fibers was unlikely.


Although the mechanism is unclear, significant autonomic dysfunction can occur during RFA. Sinus bradycardia or arrest can occur during slow-pathway modification of the AV node.


Address for reprints: Nilesh Mathuria, MD, 1 Baylor Plaza, MS 285, Houston, TX 77030 E-mail: moc.liamg@airuhtamhselin


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