electrocardiogram olthe month

Rapid Atrial Fibrillation with Left Bundle Branch Block

Pattem In a Patient with Ebsteln's Anomaly*
R. Y. C. Wang, M.B.B .S.; P. K. Lee, M.B.B .S.; and
P. H. C. Wong, M.B .B.S. , F.C.C.P.

Ee-threatening atrial fibrillation with rapid ventricu-
lar response is occasionally encountered in preex-
citation syndrome with a short refractory period of the
atrioventricular bypass tract. 1 Diagnosis of the classic
Wolff-Parkinson-White syndrome is usually obvious
from the presence of the delta wave and the short P-R
interval during sinus rhythm.
This report describes a patient with Ebstein's anom-
aly suffering from rapid atrial fibrillation with left
bundle branch block pattern. Digoxin therapy acceler-
ated the ventricular response, but quinidine restored
sinus rhythm. The ECG during sinus rhythm showed a
normal P-R interval with the same left bundle branch
block morphology. Such ECG findings in a patient
with Ebstein's anomaly would suggest the presence of a
nodoventricular fiber. 2 Electrophysiology study dem-
onstrated a constant A-V interval with both pro-
grammed atrial premature stimulation and rapid atrial
pacing. The findings were suggestive of an accessory
pathway completely bypassing the A-V node.
CASE REPORT

*From the Department of Medicine, University of Hong Kong. A 38-year-old man was first admitted in 1975 with sudden onset of
Reprint requests: Dr: Wang, Department of Medicine , Queen Mary fast, irregular palpitation. An ECG showed atrial fibrillation, with
Hospital, Hong Kong rapid ventricular rate of 180/min, and left bundle branch block

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FIGURE 1. Twelve-lead ECG during rapid atrial fibrillation.

814 Rapid Atrial Fibrillation {Mang, Lee, Motltlg)

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FIGURE 2. 1\velve-lead ECG during sinus rhythm.

pattern (Fig 1). Cardiovascular examination revealed normal heart
sounds and no murmur. The chest roentgenogram was normal. A
single DC shock of 100 J restored sinus rhythm with normal P-R
interval and the same left bundle branch block morphology (Fig 2).
Further investigation was suggested, but the patient defaulted
I.Ollow-up. He remained well until his second admission in 1982 with
a similar attack of atrial fibrillation. A loading dose of 1 mg of digoxin
was given over 24 hours, with further increase in ventricular rate.
Because of the extremely short R-R intervals (minimum, 240 msec)
during atrial fibrillation, we suspected that the patient might have an
accessory A-V pathway. Digoxin therapy was stopped, and quinidine
bisulfate, 400 mg twice daily, was given. On the next day, the ECG
confirmed reversion to sinus rhythm. liM:Hiimensional echocar-
diography revealed the presence of Ebstein's anomaly with down-
ward displacement of the septal leaflet of the tricuspid valve into the
right ventricle. The well-known association of Ebstein's anomaly
with accessory bypass tracts made the diagnosis of preexcitation even
more likely in this case. Electrophysiology study was then carried
out. No His spike could be obtained despite repeated manipulation
of the His bundle catheter around the tricuspid orifice. The A-V
interval was 100 msec and remained constant, with programmed
premature atrial stimulation up to a coupling Interval of 350 msec
(Fig 3). No ventricular response was initiated at coupling intervals
<300 msec. With incremental atrial pacing, the same phenomenon
was observed. The A-V interval was constant at various rates of atrial
pacing without any change in QRS morphology. When 2:1 A-V block

FIGURE 3. Single atrial premature stimulation at a coupling interval (S,-SJ of 350 msec. HI, HII
recordings from His bundle catheter; HRA = high right atrial electrogram.

CHEST I 83 I 5 I MAY, 1983 815

 H1
Hll
Hill
FIGURE 4. Rapid atrial pacing at a cycle length (SS) of270 msec. HI, Hll, Hlll = recordings &om His bundle
catheter.
occurred at a pacing cycle length of 270 msec, it still remained
unchanged at 100 msec (Fig 4). Ajmaline, 50 mg given intravenously
CMir three minutes, produced no change in the QRS morphology or
in the A-V interval. 'Ihus, the patient had either an A-V accessory
pathway or a nodoventricular &her which functionally bypassed the
A-V node completely. 'Ihe patient was subsequently discharged
receiving quinidine bisulfilte.
DISCUSSION
This patient's ECGs are interesting. Clinically, the
short R-R intervals during atrial fibrillation led to the
suspicion of an underlying accessory A-V pathway.
However, there was no other clue in the ECG to
suggest preexcitation; the P-R interval was nonnal
during sinus rhythm, and there was no obvious delta
wave during both sinus rhythm and atrial fibrillation.
The diagnosis of Ebstein's anomaly further confused
the issue. The typical ECG findings in this condition
include peaked P wave, low-voltage QRS complexes
with right bundle branch block. and occasionally
Wolff-Parkinson-White type B pattern. 3 Recently,
nodoventricular Mahaim fibers have been reported to
be associated with this condition. Characteristically,
such patients display various degrees of apparent left
bundle branch block during sinus rhythm or re-
ciprocating tachycardia.• The ECGs of our patient
would favor the diagnosis of a nodoventricular fiber.
Theoretically, there is always some A-V nodal delay
above the nodoventricular fiber, and digoxin, which
prolongs A-V nodal conduction, should be effective in
controlling the ventricular response. However, our
patient showed further increase in ventricular rate
with digoxin therapy, suggesting that the accessory
pathway arose in or above the proximal part of the A-V
node and behaved like an A-V bypass tract.
UnfOrtunately, the exact location of the accessory
111
pathway cannot be identified because of failure to pick
up the His bundle electrogram during electrophysiol-
ogy study. This is probably due to total preexcitation in
the basal state with the His spike buried in the QRS
complex. This postulation also explains the constant
A-V interval and the lack ofchange in QRS morphology
during premature atrial stimulation and rapid atrial
pacing. Although we are uncertain about the exact
anatomic nature of the accessory pathway in our
patient, it functionally bypasses the A-V node com-
pletely. This infOnnation is ofgreat clinical importance.
Digoxin may further enhance conduction along an A-V
bypass tract and precipitate ventricular fibrillation. 4
Quinidine is a more appropriate drug for this condi-
tion. 5 Also, this patient illustrates the protean nature of
Ebstein's anomaly. The diagnosis ofEbstein's anomaly
is obvious in patients with typical physical signs and
roentgenographic and ECG features. But it can be
c:liflicult in patients at the other end of the spectrum,
where none of these typical findings is present.
REFERENCES
1 Gallagher JJ, Pritchett ELC, Sealy WC, Kasell J, Wallace AG. 'Ihe
preexcitation syndromes. Progr Cardiovasc Dis 1978; 20:285-327.
2 Smith WM, Gallagber JJ, Kerr CR, seaiy WC, Kasell JH, BeDIOD
OW, et al. 'Ihe electrophysiologic basis and management of
symptomatic recurrent tachycardia in patients with Ebstein's
anomaly of the tricuspid valve. Am J Cardiol1982; 49:1223-34.
3 Giuliani ER, Fuster V, Brandenburg RO, Mair DO. Ebstein's
anomaly: the clinical katures and natural history of Ebstein's
anomaly of the tricuspid valve. Mayo Clin Proc 1979; 54:163-73
4 Sellers TO Jr; Bashore TM, Gallagher JJ. Digitalis in preexcitation
syndrome: analysis during atrial &brillation. Cinrulation 1977;
56:260-66
5 Sellers TO Jr; Campbell RWF, Bashore TM, Gallagher JJ. Effects
of procainamide and quinidine sulfilte in the Wolft'-Parkinson-
White syndrome. Cinrulation 1977; 55:15-22