Ventriculoatrial conduction in complete atrioventricular block ☆ Miguel A. Arias, MD, PhD, ⁎ Jesús Jiménez-López, MD, Marta Pachón, MD, Miguel Jerez-Valero, MD, Alberto Puchol, MD, Luis Rodríguez-Padial, MD, PhD Cardiac Arrhythmia and Electrophysiology Unit, Department of Cardiology, Hospital Virgen de la Salud, Toledo, Spain Received 6 February 2012 Abstract The case of a patient with complete atrioventricular block with capability of rapid ventriculoatrial conduction with unusual behavior is presented. Potential mechanisms are discussed. © 2012 Elsevier Inc. All rights reserved. Keywords: Atrioventricular conduction; Cardiac pacing Case presentation A 60-year-old man with syncopal complete atrioventric- ular (AV) block with ventricular escape rhythm of approximately 20 beats per minute in the setting of chronic ischemic cardiomyopathy, PR interval of 225 milliseconds plus right bundle branch block (RBBB) and left anterior fascicular block (LAFB), and severely reduced left ventric- ular systolic function underwent a dual-chamber defibrillator implant (Guidant Vitality 2 DR model T165, St. Paul, MN, USA) several year before. The device was programmed to the DDD mode. During the following years, the patient underwent routine 6 monthly follow-up visits. Device interrogations always revealed pacemaker dependency with complete AV block and no escape ventricular rhythm above 30 beats per minute when the base paced rate was decreased to 30 ppm in the VVI mode (Figure 1A). However, incremental ventricular pacing (VVI mode) demonstrated a retrograde 1:1 ventriculoatrial (VA) conduction capacity of at least (explored) 150 ppm (Figure 1B). To rule out the presence of a concealed AV accessory pathway, a bolus of 12 mg of intravenous adenosine was administered (Figure 1C) during VVI pacing at 90 ppm with subsequent transient VA dissociation. Just after adenosine infusion, the device was reprogrammed to VVI mode at 30 ppm, and 1:1 AV conduction was observed (Figure 1D). Resumption of AV conduction occurred 20 minutes after that, when the sinus rate was approximately 65 beats per minute. What is the most likely mechanism? Commentary The occurrence of VA conduction in patients with AV block can be mainly related to the following mechanisms: (a) VA conduction through the normal conduction system and (b) presence of a concealed AV accessory pathway. In general terms, the capability of VA conduction is mainly related to the presence and quality of antegrade conduction. Although it is well known that AV conduction is better than VA conduction in most patients at the same paced rates, it is possible to observe the presence of VA conduction in patients with complete AV block even in the absence of a concealed accessory pathway. Some authors have identified that it can occur mainly if block is located beyond the bundle of His and the AV node is intact; it is though that, in such cases, the retrograde pathway around the block to the AV node may be by muscular conduction. 1,2 For that reason, patients with very prolonged PR intervals are much less likely to demonstrate VA conduction. In the present case, the history of intraventricular conduction disease (right bundle-branch block plus LFAB) with a not-too-prolonged PR interval will suggest a level of antegrade block below the AV node. The observed response to adenosine infusion adds interesting information to the case. The intravenous bolus of adenosine resulted in transient VA dissociation, indicat- ing the involvement of adenosine-sensitive tissue in the VA conduction, likely the AV node, and therefore makes unlikely the presence of a concealed AV accessory pathway as it has minimal effect on accessory pathway conduction. Moreover, after adenosine administration, a slight increase in the sinus rate with resumption of 1:1 AV conduction was observed. This finding may be caused by reflex activation of the sympathetic nervous system with a rapid increase in catecholamine levels caused by adenosine that improved conduction properties in the AV node. Increases of the Available online at www.sciencedirect.com Journal of Electrocardiology 45 (2012) 391 – 393 www.jecgonline.com ☆ Conflict of Interest: None. ⁎ Corresponding author. Unidad de Arritmias y Electrofisiología Cardiaca Avda. Barber 30, Planta Semisótano, 45004, Toledo, Spain. E-mail address: maapalomares@secardiologia.es 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.03.005