Discussion:
Concealed His extrasystoles mimicking AV block was first described by Langendorf and Mehlman in 19471. The mechanism was postulated to be secondary to His extrasystoles that fail to conduct to the ventricle but partially conduct into the AV junction. This was later confirmed in an electrophysiology study (EPS) in 1970 by Rosen et al2. AV block secondary to His extrasystoles has been termed pseudo AV block. This phenomenon was well documented in the 1970s3-5. There have been few scattered case reports since then. In this case report, we present an otherwise healthy 46-year-old female who was found to have 156 episodes of second-degree Mobitz II AV block on ambulatory monitoring for palpitations. Evaluation for reversible causes with Lyme titers, transthoracic echocardiogram, cardiac MRI, and treadmill exercise stress test were unremarkable. However, ECG during her stress test provided insight into the cause of her AV block. ECG in Figure 3 showed sinus tachycardia, junctional bigeminy with RBBB, and a blocked sinus P wave that was closely coupled to a small negative deflection consistent with an atrial depolarization from a His extrasystole that conducted retrogradely to the atrium but failed to conduct to the ventricle and partially conducted into the AV node resulting in a pseudo AV block. This occurrence was supported by the observation of frequent junctional bigeminy that conducted with RBBB. At a shorter coupling interval, a His extrasystoles likely blocked antegrade in the His Purkinje system and failed to depolarize the ventricles. In addition, it also conducted retrograde into the slow AV node pathway resulting in retrograde atrial activation and into the fast AV node pathway causing the preceding sinus beat to block in the AV node (pseudo-AV block) as illustrated in Figure 4.
In 1973, Narula and Eugster et al. suggested that AV block from His extrasystoles could be a sign of conduction disease distal to the His bundle in some patients indicating the need for a pacemaker6-7. However, in 1976, Booner and Zipes showed no evidence of distal conduction disease in some patients with pseudo AV block9. While we cannot rule out with absolute certainty the presence of distal conduction system disease in this case without an electrophysiology study, the likelihood of distal disease islow for the following reasons. At baseline, this patient had normal PR interval and QRS duration. Second, she had no AV block at peak exercise (153 bpm). These findings along with her frequent ectopy were supportive of pseudo AV block secondary to concealed His extrasystoles as opposed to distal conduction system disease. After a lengthy conversion with the patient, electrophysiology study was deferred and Flecainide was started. While there have been no reported case studies of using Class IC antiarrhythmics to treat His extrasystoles, we chose Flecainide based on the results of previous studies using other class I antiarrhythmic agents as shown in Table 1. Five months after initiation of Flecainide, a repeat ambulatory ECG recording showed no AV block. Patch monitor showed rare PACs and PVCs. A repeat treadmill stress test showed rare junctional complexes without AV block.
The findings in this patient underscore the fact that concealed His extrasystoles can be diagnosed from careful analysis of the surface electrocardiogram, and Flecainide is an effective treatment for pseudo AV block from concealed His extrasystoles. Treatment of pseudo AV block from His extrasystoles with class I antiarrhythmic agents is summarized in Table 1.