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Brief description/objective

Case description
A 79-year-old male was admitted to our outpatient
clinic with symptomatic heart failure (HF). The patient
reported impaired exercise tolerance with increasing
shortness of breath in the previous 4 weeks and a
weight gain of 5 kg. The ECG showed new onset atrial
fibrillation (AF) with rapid conduction and preexisting
left bundle branch block (fig. 1). The patient had a history
of coronary artery disease with successful PCI
of the LCX after inferolateral myocardial infarction
15 months previously. Medication consisted of acetylsalicylic
acid, torasemide, and atorvastatin. Physical
examination revealed positive hepatojugular reflux,
normal blood pressure (110/85 mm Hg), irregular heart
beat (approx. 110 at rest), and right sided pleural effusion.
Echocardiography showed severely reduced left
ventricular ejection fraction (15–20%) with signs of left
ventricular dyssynchrony, moderate mitral regurgitation
and severe tricuspid regurgitation.
Figure 1 shows the patient’s resting ECG; figure 2
shows a sequence of a 24-hour Holter ECG.
...
Questions
1. What do you see on the left and what on the right
side of the ECG (fig. 2)?
2. How do you explain the morphology of the 3rd QRS
complex (fig. 2, arrow)?
Answers
1. The first two QRS complexes show atrial fibrillation
with bundle branch block pattern, which differs
slightly from that of the resting ECG (fig. 1 – probably
due to different lead placement of the Holter electrodes).
The 4th to 7th QRS complexes show a right bundle
branch block pattern with inferior axis at a heart rate
of 112 bpm, which is slightly irregular (repeated
episodes with similar morphology have been observed
in the 24-hour ECG with heart rates ranging from 110
to 133 bpm). In consideration of the preexisting conduction
abnormalities, a frequency-dependent change
in aberration cannot be excluded, although other explanations
are more likely. In a patient with severely
impaired LVEF and a past history of MI the most important
differential diagnosis is non-sustained ventricular
tachycardia (VT; also according to the Brugada criteria
R/S interval in one precordial lead >100 ms). As
an important differential diagnosis, accelerated idioventricular
rhythm (AIVR) must be considered. Interestingly,
there is no consensus on the upper rate limit
for the definition of AIVR; it is usually defined as a
heart rate between 100 and 120 bpm [1]. The fact that
faster episodes with similar QRS morphology could
also be observed would favour VT; however, in view of
the irregularity of the tachycardia, we rather assumed
AIVR.
2. Interestingly, the 3rd complex shows a narrow
QRS complex which contrasts with the broad left bundle
branch pattern on the left and the right bundle
branch pattern on the right. This feature is consistent
with a fusion beat between these two different bundle
branch morphologies, leading to fusion-induced resynchronisation
of this single beat. Fusion beats are common
in AIVR as well as in VTs.
Since NYHA III dyspnoea persisted despite optimised
medical therapy, including appropriate rate control,
our patient qualified for the implantation of an
ICD/CRT device. In this case, the “electrical aim” of
resynchronisation would have been to achieve a QRS
complex similar to the fusion beat shown in the middle,
although it must be admitted that QRS width has
proved to be a poor predictor of CRT response [2].
References
1 Grimm W, Hoffmann J, Menz V, Schmidt C, Müller HH, Maisch B. Significance
of accelerated idioventricular rhythm in idiopathic dilated
cardiomyopathy. Am J Cardiol. 2000;85(7):899–904, A10.
2 Jia P, Ramanathan C, Ghanem RN, Ryu K, Varma N, Rudy Y. Electrocardiographic
imaging of cardiac resynchronization therapy in heart
failure: observation of variable electrophysiologic responses. Heart
Rhythm. 2006;3(3):296–310.