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.