Selective sinoatrial suppression during post-ablation adenosine testing without atrioventricular block

A 45-year-old male presented with symptomatic orthodromic atrioventricular (AV) receprocating tachycardia (AVRT) mediated by a left lateral accessory pathway (AP). He underwent successful radiofrequency (RF) ablation, with acute success confirmed by the loss of pre-excitation and retrograde AP conduction. To definitively exclude residual AP conduction, a post-ablation adenosine challenge (12 mg IV push) was performed; unexpectedly, instead of the typical brief AV block (Figure 1A,B), the patient developed sinus node dysfunction (SND) manifesting as a period of sinus slowing. To rule out inadequate intravenous delivery as the cause of the initial response, an 18 mg dose of adenosine was administered again. This higher dose reproduced the same isolated sinus node suppression without AV block. The baseline sinus node function was normal. Post-ablation decremental AV conduction, a slight but insignificant prolongation of the atriohisian (AH) interval (65 to 75 ms) following adenosine administration, and the presence of ventriculoatrial dissociation (Figure 1C) collectively rendered an AH AP an unlikely diagnosis. (A) Post-ablation adenosine challenge (12 mg IV push) caused sinus node dysfunction without affecting atrioventricular nodal conductivity (Not shown: Post-ablation study revealed a baseline Atriohisian (AH) interval of 65 ms and a His-ventricle (HV) interval of 40 ms at a sinus cycle length of 770 ms. Incremental atrial pacing demonstrated decremental nodal conduction, evidenced by a progressive AH interval prolongation, leading to atrioventricular Wenckebach periodicity at a cycle length of 290 ms. Atrial extrastimulus testing corroborated these findings, showing similar decremental behaviour with AH block occurring at S1: S2 of 450:230 ms. The AH interval in the last conducted beat of this sequence measured 159 ms. Dual AV nodal physiology was ruled out); (B) Enlarged view showing sinus slowing without significant change in AH or HV intervals; (C) Ventriculoatrial dissociation during ventricular burst pacing showing no evidence of retrograde accessory pathway conduction. Adenosine exerts its negative dromotropic effects primarily through the activation of the A1 receptor (A1R), leading to a direct (cAMP-independent) activation of the inwardly rectifying potassium currents, specifically IK Ado, Ach.1–3 A1R heterogeneity (relative abundance of A1R in different cardiac structures; internodal and intranodal heterogeneity) may represent the sole cause for varying sensitivities to intravenous adenosine. This observation may partially account for the occasional therapeutic failure of adenosine in managing AV node-dependent supraventricular tachycardias. However, detailed studies on the comparative A1R density between the sinoatrial (SA) and AV nodes remain limited. In summary, this case highlights rare, selective SA node sensitivity to adenosine that spares the AV node, which potentially complicates the accurate assessment of ablation success via adenosine challenge. Given the probable transient nature of this phenomenon, the requirement for pacing or atropine is considered low, and a repeat adenosine challenge is likely redundant. Sudipta Mondal (Conceptualization [equal], Formal analysis [lead], Writing—original draft [equal], Writing—review & editing [lead]), Nadeem Afroz Muslim (Conceptualization [equal], Formal analysis, Writing—original draft [equal], Writing—review & editing) We extend our sincere gratitude to Subhajit, Nayan, and Sourav for their active participation in this case and for their successful efforts in retrieving the necessary data. Consent: Obtained from the patient in line with COPE guidance. None declared. No new data were generated or analysed in support of this research. Not applicable as it is an anonymous case report.