Brugada pattern induced by tricyclic antidepressant

A 31 year old male presented obtunded after a suspected intentional overdose with amitryptiline.  He was intubated, and this ECG was recorded:

Time zero: QRS duration = 162 ms, QRS axis = 147.  There is a wide QRS and large R-wave in lead aVR, typical of amitryptiline toxicity.  But the ECG also looks like classic type I Brugada pattern, in V1 and V2 but especially in V2: there is an rSR' with downsloping ST elevation.

After immediate intravenous bicarbonate, this ECG was recorded 14 minutes later:

Time 14 minutes: after 100 ml of 8.4% bicarbonate: QRS = 146 ms.  The QRS has narrowed slightly.  The Brugada pattern is still present


At 2 hours, after more bicarbonate, this was recorded:

Time = 2 hours, after more bicarbonate: QRS = 117 ms.  There is still a hint of Brugada pattern in V1.


Day 4 this was recorded:

Again, there is a hint of Brugada in V1, and even moreso in V2, with rSR' and downsloping ST elevation.

Day 5 this was recorded:

Still a hint of Brugada in V1

One month later:

Normalized

When the patient awoke, he and his family reported a family history of close relatives with cardiac arrest of uncertain etiology.  The patient himself had never had syncope or dysrhythmias.  Without Brugada pattern on the baseline ECG, there is no Brugada syndrome.  However, there is an uncertain history of sudden death as well as inducible Brugada pattern.

There is no clear management solution for such patients.  The electrophysiologist was of the strong opinion that an IVCD was not indicated without further information.  The management of inducible type I Brugada pattern is not at all clear.

The electrophysiologist felt that if the pattern was also inducible with procainamide, then genetic testing would be indicated.  If not, then avoidance of the TCA would be enough.  He proceeded also with an implantable loop recorder to detect subclinical dysrhythmias, and this was negative.

Drug-Induced Brugada Syndrome

Suffice it to say that this is a very complex topic and I know little more about it than can be read in this 2009 article from Europace, the most recent article I could find on the topic.  It is free full text.    http://europace.oxfordjournals.org/content/11/8/989.full.pdf+html

Here are a very few salient points from the article:

Brugada syndrome is due to a genetic defect in the gene (SCN5A) that codes for tha alpha unit of the sodium channel.  There appear to be many kinds of defects with variable manifestations and penetrance, and variable susceptibility to drugs, including TCAs (or also to other states such as fever).

TCAs even at therapeutic doses have been reported to unmask latent Brugada, and such reported cases have polymorphism of the gene.