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