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952

Arrhythmia Rounds
Section Editor: George J. Klein, M.D.

Different Narrow QRS Morphologies


in the Surface ECG: What is the Mechanism?
LUCIO CAPULZINI, M.D., GAETANO PAPARELLA, M.D.,
GIAN BATTISTA CHIERCHIA, M.D., CARLO DE ASMUNDIS, M.D.,
ANDREA SARKOZY, M.D., and PEDRO BRUGADA, M.D., Ph.D.
From the Heart Rhythm Management Center, UZ Brussel-VUB, Brussels

Case Presentation

Discussion

A 16-year-old female with a long history of rapid, regular,


recurrent palpitations with documentation of a tachycardia
with left bundle branch block (LBBB)-like QRS complex
(Fig. 1) was referred to our center for an electrophysiological
study. The patient had no structural heart disease and her
baseline ECG is shown in Figure 2. Based on the baseline
ECG and the clinical history, which tachycardia mechanisms
would you suspect?

The baseline 12-lead ECG reveals sinus rhythm without


clear ventricular preexcitation. But, a better analysis of the
ECG reveals different narrow QRS complex morphologies.
Continuous recording of lead II shows 3 QRS complex morphologies (arrow, Fig. 2). The first QRS complex shows an
Rs pattern; the 2nd, 3rd, and 4th QRS show an rs pattern;
the 5th QRS complex is a slightly wider (QRS width, 100 ms)
with a Qr pattern. Then, the first pattern occurs again in
the following beats. Changes in QRS complex morphology
are also well recognizable in leads I, III (2nd beat), and precordial leads V1V3 (5th beat). The most evident change in
peripheral leads, with an rS pattern, when compared with
the 1st beat is seen in lead III. The precordial leads V1V3
show an incomplete LBBB-like QRS complex morphology
(QRS width, 100 ms). Different PR intervals precede all these
different QRS morphologies. The PR interval is 150 ms in

J Cardiovasc Electrophysiol, Vol. 20, pp. 952-954, August 2009.


Address for correspondence: Lucio Capulzini, M.D., Heart Rhythm Management Center, UZ Brussel-VUB, Laarbeeklaan 101, 1090 Brussels,
Belgium. Fax: 0032 477 68 40; E-mail: luciomassimo@hotmail.com
doi: 10.1111/j.1540-8167.2008.01429.x

Figure 1. The clinical tachycardia documented in this patient.

Capulzini et al.

Arrhythmia Rounds

953

Figure 2. Resting 12-lead ECG.

the 1st beat and 130 ms in the 2nd, 3rd, and 4th beats. The
PR interval shortens to 100 ms in the 5th beat.
The differential diagnosis of this ECG should include:
(1) late ventricular premature beats, and (2) intermittent and
variable degree of preexcitation.
Intermittent and variable degree of intraventricular aberrant conduction is excluded because of the shortening of the
PR interval associated to the wider QRS complexes.
The possibility of late ventricular premature beat cannot
be excluded from this tracing. A variable degree of fusion
between a normally conducted beat and a late ventricular
extrasystole can, indeed, result in this pattern.
A mechanism that certainly has to be considered is intermittent and variable ventricular preexcitation. The rS

pattern in lead III of the "preexcited" beats has to suggest


an atriofascicular (AF) fiber in this patient with paroxysmal
rapid tachycardia. The incomplete LBBB-like QRS complex
preceded by a short PR in the fifth beat, in this case, should
likely be explained by a sudden enhanced conduction over
the AF pathway or by automaticity arising in the AF pathway,
which has been occasionally described.1,2
AF fibers are uncommon but a very distinct form of accessory pathway (AP), comprising less than 3% of all APs.
These APs arise from the right atrium at the parietal tricuspid ring and terminate in or near the distal right bundle
branch (AF pathway) or less frequently, in the right ventricle near the tricuspid annulus (AV pathways). They exhibit
slow and exclusively anterograde decremental conduction.3

Figure 3. Atriofascicular pathway potential (arrows) identified at the 9 oclock position on the tricuspid valve as seen from the left anterior oblique
projection.

954

Journal of Cardiovascular Electrophysiology Vol. 20, No 8, August 2009

Sporadic cases of left-sided anterograde decremental pathway have been reported.4,5 It should be stressed that in these
patients there is no classic delta wave. ECG signs of ventricular preexcitation may become evident only during antidromic
tachycardia. Because of the right-sided location of these pathways, preexcited QRS complexes demonstrate LBBB-like
morphology.
The surface ECG in the presence of an AF fiber has shown
minimal preexcitation in up to 30% of patients.6,7 Apart from
the absence of q waves in the left precordial leads, no specific QRS complex pattern has been described.8 In 2004,
Sternick et al.9 reanalyzed a large series of patients with
AF fibers. They found that the rS pattern in lead III on
many ECGs, considered as normal in previous studies, were
associated with AF APs. This minimal preexcitation was
found in 60% of the patients reexamined.9 In their study they
also noted variability of minimal preexcitation on the same
ECG in 2 patients. Variability in preexcitation is consistent
with different degrees of fusion due to conduction over both
the normal AV conduction system and a decremental AP.
Thus, this is exactly what we found in our ECG and suggested to us a diagnosis of an AF pathway considering the
association with the LBBB morphology during the clinical
tachycardia.
The patient underwent an EP study and pacing maneuvers during tachycardia confirmed the presence of an AF
fiber. An AF pathway potential (arrows, Fig. 3) was identified at the 9 oclock position on the tricuspid valve in the
left anterior oblique projection, and successful ablation was
performed. After 2 months of follow-up the patient is free

of symptoms and the control surface ECG is completely


normal.
References
1. Klein GJ, Guiraudon GM, Kerr CR, Sharma AD, Yee R, Szabo T, Wah
JA: "Nodoventricular" accessory pathway: Evidence for a distinct accessory atrioventricular pathway with atrioventricular node-like properties.
J Am Coll Cardiol 1988;11:1035-1040.
2. Heald SC, Davies DW, Ward DE, Garratt CJ, Rowland E: Radiofrequency catheter ablation of Mahaim tachycardia by targeting Mahaim
potentials at the tricuspid annulus. Br Heart J 1995;73:250-257.
3. Josephson ME: Clinical Cardiac Electrophysiology, Third ed. Philadelphia: Lippincott Williams and Wilkins; 2002: 402-408.
4. Golberg JJ, Pederson DN, Damle RS, Kim YH, Kadish AH: Antidromic tachycardia utilizing decremental, latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia. J Am Coll Cardiol 1994;24:732-738.
5. Tada H, Nogami A, Naito S, Oshima S, Tanigichi H, Kutsumi Y: Left
posteropseptal Mahaim fiber associated with marked longitudinal dissociation. PACE 1999;22:1696-1699.
6. McClelland JH, Wang X, Beckman KJ, Hazlitt HA, Prior MI, Nakagawa H, Lazzara R, Jackman WM: Radiofrequency catheter ablation of
right atriofascicular (Mahaim) accessory pathways guided by accessory
pathway activations potentials. Circulation 1994;89:2655-2666.
7. Bardy GH, Fedor JM, German LD, Gallagher JJ: Surface electrocardiographic clues suggesting presence of a nodofascicular Mahaim fiber. J
Am Coll Cardiol 1984;3:1161-1168.
8. Haisseguerre M, Cauchemez B, Marcus F, Le Metayer P, Lauribe P,
Poquet F, Gencel L, Clementy J: Characteristics of the ventricular insertion sites of accessory pathways with anterograde decremental conduction propreties. Circulation 1995;91:1077-1085.
9. Sternick EB, Timmermans C, Sosa E, Cruz F, Rodriguez LM, Fagundes
M, Gerken LM, Wellens HJ: The electrocardiogram during sinus rhythm
and tachycardia in patients with Mahaim fibers: The importance of an
rS pattern in lead III. J Am Coll Cardiol 2004;44:1626-1635.

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