And what about the ECG: Difference between revisions

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m (New page: {{NHJ| |mainauthor= '''A.A.M. Wilde, R.H.J. Peters''' |edition= 2006:09,315 }} Figure 1|thumb A 63-year-old lady presented with episodic chest pain wi...)
 
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[[Puzzle_2006_9_315 Answer|Answer]]
[[Puzzle_2006_9_315 Answer|Answer]]
At first glance the ECG shows a sinus rhythm of 53
beats/min (RR 1140 according to the computer
analysis). The electrical axis is vertical (95°). The PQ
interval is slightly prolonged (220 msec). The QRS
width is within normal limits. Repolarisation is grossly
abnormal and significantly prolonged. In the first
complex of lead aVL, for example, it measures 600 ms
(QTc 567 ms).
A second look at the ECG suggests the presence of
a double P-wave frequency, best seen in the usual leads
where sinus P waves are most prominent, i.e. lead II
(rhythm strip) and lead V1. Hence, the correct diagnosis
should be a sinus rhythm of 106 beats/min, 2:1
atrioventricular block and significant QT prolongation.
The AV block worsened episodically during telemetry
recording.
The question that now should arise is whether the
QT prolongation is congenital or acquired. Different
factors causally involved in acquired LQTS were not
present, except for the female gender and the slight
bradycardia. However, the latter is not very pronounced
and most likely caused by a functional AV
block. The second P wave is not able to conduct
through the AV node because the ventricles are still
refractory secondary to the prolonged QT interval.
This electrocardiographic appearance actually makes
a congenital QT prolongation far more likely.
In conclusion,''' this ECG suggests the presence of an apparent asymptomatic congenital LQTS'''. Since the
bradycardia plays an important role, DDD-PM
implantation is warranted as well as DNA diagnostics.
The latter should primarily be directed at the SCN5a
gene, the gene encoding the cardiac sodium channel
and involved in long-QT syndrome, Brugada syndrome
and conduction disorders.

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