Pause-Dependent Paroxysmal Episode of Third-Degree Atrioventricular Block Triggered by Premature Atrial Contraction

Introduction

Paroxysmal third-degree atrioventricular block (AVB) is clinically characterized by a sudden change from 1: 1 atrioventricular (AV) conduction leading to complete AVB. Patients can exhibit a vast array of symptoms, but commonly, paroxysmal AVB leads to presyncope, syncope, or possibly sudden cardiac death. Here, we present the case of a 65-year-old man with frequent episodes of presyncope and syncope for 3 weeks; a diagnosis of pause-dependent paroxysmal AVB was made. The patient received a dual-chamber pacemaker, and during the 2-year follow-up, the patient was free of presyncope and syncope.

Case Report

A 65-year-old man with frequent episodes of presyncope and syncope for 3 weeks was admitted to our hospital for further diagnosis. He had no history of myocarditis, cardiomyopathy, or other heart disease and denied a family history of coronary heart disease or sudden cardiac death. He had not received any antiarrhythmic medication and had no history of catheter ablation before admission to the hospital. Echocardiography revealed that all 4 cardiac chambers and dual ventricular functions were normal. A resting 12-lead electrocardiogram (ECG) showed an incomplete right bundle branch block with a PR interval of 232 ms and a QRS duration of 108 ms (Figure 1). The 24-h Holter recording revealed multiple episodes of third-degree AVB. Figure 2 shows 1 episode of pause-dependent paroxysmal third-degree AVB, with a ventricular asystole of 13.2 s. Based on the intracardiac tracing data shown in Figure 3, the baseline atrial-His interval was 77 ms, and the His-ventricular interval was 58 ms for the first 2 beats. The nonconducted premature atrial contraction (PAC) triggered another episode of third-degree AVB, and ventricular asystole was terminated by pacing. What is the likely mechanism of third-degree AVB?

Discussion

Figure 1 shows the ECG characteristics of an incomplete right bundle branch block and first-degree AVB, with a PR interval of 232 ms, indicating potential conduction disease in the AV node, His bundle, or infra-Hisian-Purkinje system. Figure 2 illustrates a transition from an apparently normal AV 1: 1 conduction to a transient episode of third-degree AVB, which was triggered by a nonconducted PAC and a subsequent P-P pause of 1260 ms, leading to a ventricular asystole of 13.2 s. During this ventricular asystole, no ventricular escape occurred, indicating that the site of the block was very low, in other words, at or distal to the infra-Hisian-Purkinje system. As shown in Figure 3, due to the short coupling interval of this nonconducted PAC, a functional conduction block occurred at the AV node (phase 3 block); consequently, no His potential could be recorded. After a long P-P pause of 910 ms triggered by the nonconducted PAC, a pause-dependent AVB was perpetuated for 5 cycles. This pause-dependent AVB could be explained by a phase 4 block that occurred in the diseased distal infra-Hi-sian-Purkinje system, as evidenced in the tracing by the presence of a His potential after each atrial activation [1].

Phase 3 and phase 4 blocks are generally differentiated by the mechanisms of the conduction blocks in the AV node and the His-Purkinje system, respectively. The phase 3 block, also known as tachycardia-dependent AVB, is a physiological or functional block that can occur in the normal AV node or the His-Purkinje system after a PAC or at the beginning of a supraventricular tachycardia in the normal heart. The phase 4 block, also known as bradycardia-dependent AVB, occurs mostly in the diseased AV node and the His-Purkinje system. Pause-dependent paroxysmal AVB has been reported to be both bradycardia (phase 4 block) and tachycardia dependent (phase 3 block) [2,3]. A brady-cardia-dependent (phase 4) block can sometimes occur in combination with a tachycardia-dependent (phase 3) block. In this situation, there is a relatively narrow range between the critical heart rates for the development of phase 4 and phase 3 blocks, where normal AV conduction can occur. Rosenbaum et al proposed a model in which the entrance block and phase 4 block in the diseased conducting system play major roles in the development of bradycardia-dependent bundle branch block [4]. Several studies have shown that a bundle branch block is associated with reflex syncope or AVB in more than 40% of patients [5].

This form of AVB can be precipitated by PAC or ventricular premature beats, His bundle extrasystoles, or sinus rhythm slowing either spontaneously or induced by carotid sinus massage [6]. Typically, the relatively long runs of ventricular asystole are terminated with resumption of AV conduction by an appropriately timed escape or premature beat that resets the membrane action potential to its resting state [7]. Less commonly, as shown in our case, an increase in the sinus rate (from 941 ms to 640 ms) permits the return of 1: 1 AV conduction (Figure 2).

Conclusions

We report a case in which PAC-triggered pause-dependent paroxysmal AVB was managed via implantation of a dual-chamber pacemaker. This type of AVB is an abrupt, unexpected, repetitive block of atrial impulses as they propagate to the ventricles. It is relatively rare, and due to its transient nature, it is often under recognized and can lead to sudden cardiac death.