What is the most likely diagnosis?
We observed an irregular, wide QRS complex tachycardia induced by AES;
some of the ventricular beats presented with RBBB morphology, while
others with an LBBB pattern; and some of the atrial beats were blocked
to the ventricles. The blocked atrial impulse automatically excludes
ventricular tachycardia and atrioventricular reentrant tachycardia
(AVRT), since the ventricles are not an essential part of the circuit.
At this point, there are two possible diagnostic approaches: atrial
tachycardia (AT) or atrioventricular nodal reentrant tachycardia
(AVNRT).
It should be noted that this patient had a severe conduction system
disease, which could be confirmed by observing the HV interval. Most of
the time, the QRS has an RBBB pattern, with an HV interval of 60 ms, but
when the QRS changes to the LBBB pattern, the HV interval lengthens to
114 ms. Blocked atrial beats below the His bundle could also be seen and
are responsible for the R-R interval irregularity.
Careful observation of tachycardia activation can help establish a
correct diagnosis. First, the tachycardia induction repeatedly occurs
with an increase in the A-H interval, suggesting AVNRT as the cause of
the arrhythmia¹ ².
Additionally, we can observe that there is some variation in the A-A
interval, but it is always preceded by changes in the H-H interval,
which is not seen in ATs. Importantly, the H-H interval variation is
closely related to changes in the A-H interval, suggesting that there is
more than one slow pathway capable of antegrade conduction. The H-A
interval (retrograde conduction) remained unchanged during tachycardia
for 75 ms, suggesting that the antegrade conduction is the cause of the
H-H variation. This observation rules out AT and leaves us with AVNRT as
the cause of this patient’s arrhythmia¹ ².
We decided not to perform slow pathway ablation at that moment, due to
the risk of a complete heart block.
The patient underwent dual chamber pacemaker implantation without
complications. A few days after pacemaker implantation, the patient was
recruited in a new EPS with slow pathway ablation without complications.
An intriguing finding in this case is that the patient had persistent
palpitations after pacemaker implantation and before the slow pathway
ablation, proving that his symptoms were related to AVNRT. More than one
year after the ablation procedure, the patient remains asymptomatic and
free of antiarrhythmic drugs.
This was an atypical presentation of a typical AVNRT. The
electrogram tracings showed the exact mechanism of the arrhythmia,
thereby immediately ruling out AVRT and AT, which is the most important
differential diagnosis. We also demonstrated the mechanism by which
there is variation in the cycle length, showing that it depends on the
antegrade conduction over more than one slow pathway, as proven by the
exact lengthening of the A-H interval determining the same amount of
lengthening in the A–A and H–H intervals.
Such a unique presentation of AVNRT in the presence of significant
conduction disorders results in a challenging ECG tracing, as it would
be impossible to establish a precise diagnosis without performing an
EPS. To the best of our knowledge, this is the first report showing the
association of many electrophysiological phenomena during AVNRT, making
diagnosis by ECG difficult. The only way to determine the origin of all
ECG findings is by careful analysis of the intracavitary signals.