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E Zakynthinos, T Vassilakopoulos, C Roussos, and S Zakynthinos
Abnormal atrial and ventricular repolarisation resembling myocardial injury after tricyclic antidepressant drug intoxication
Heart 2000; 83: 353-354 [Full text] [PDF]
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[Read eLetter] Pseudo Brugada or true Brugada revealed by tricyclic agents?
De Roy   (19 May 2000)

Pseudo Brugada or true Brugada revealed by tricyclic agents? 19 May 2000
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De Roy,
Cardiologist
Arrhythmia Unit, University of Louvain, YVOIR, Belgium

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Re: Pseudo Brugada or true Brugada revealed by tricyclic agents?

deroy{at}card.ucl.ac.be De Roy

Dear Editor

We have read with great interest the short case in cardiology reported by E Zakynthinos et al (1) in the March 2000 edition of Heart. The ECG recordings after acute ingestion of amitriptyline are remarkable, especially the ST segment elevation in the precordial leads V1 - V3, 6 to 100 hours after admission in the intensive care unit.

The ECG pattern resembles markedly the ones described in the Brugada syndrome (2). Thus this case could represent a specific effect of the ionic action of tricyclic agents with selective blockade of the sodium channels (3,4), mimicking temporarily a Brugada pattern, as an acquired phenomenon in an otherwise electrically normal myocardium.

Another mechanism could be an unmasking effect of amitriptyline similar to that of other sodium channel blockers which revealed a silent dysfunction of the sodium channels in a "concealed" Brugada Syndrome (5). This has, in our opinion, to be discussed and verified by means of a pharmacological test with ajmaline (5), at distance of the acute event. The apparent absence of threatening arrhythmias in the presence of such a high concentration of amitriptyline is however an argument pleading against this hypothesis.

In the same issue of Heart, R P Steeds et al (6) report a case of abnormal ventricular conduction following dothiepin overdose with images resembling an acute myocardial infarction. The ST segment elevation in leads V1-V3 is however somewhat different and less suggestive of a Brugada Syndrome. Nevertheless, the ionic mechanism of intoxication could be the same, though occurring in an electrically otherwise normal myocardium. Similarly in this case, an ajmaline pharmacological test could be appropriate to ensure the integrity of sodium ionic channels. A genetic study would be also advocated in these two cases.

L DE ROY, MD
C SCAVEE, MD
J MUCUMBITSI, MD
D BLOMMAERT, MD
Department of Cardiology, Arrhythmia Unit
University of Louvain
B 5530 YVOIR Belgium

References

1. E. Zakynthinos, T. Vassilakopoulos, C. Roussos, S Zakynthinos. Abnormal atrial and ventricular repolarisation resembling myocardial injury after tricyclic antidepressant drug intoxication. Heart 2000;83:353-354.

2. P Brugada, J Brugada. Right bundle-branch block persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report J Am Coll Cardiol 1992;20:1391-1396.

3. MJ Barber, CF Starmer, AO Grant. Blockade of cardiac sodium channels by amitriptyline and diphenylhydantoïne.Evidence for two use-dependent binding sites. Circ Res 1991;69:677-96.

4. C Nau, M Seaver, SY Wang, GK Wang. Block of human heart hH1 sodium channels by amitriptyline.J Pharmacol Exp Ther 2000;292:1015-23.

5. R Brugada, J Brugada, C Antzelevitch, G E Kirsch, D Potenza, J A Towbin, P Brugada: Sodium channel blockers identify risk for sudden death in patients with ST segment elevation and right bundle branch block but structurally normal hearts. Circulation 2000;101:510-515.

6. R P Steeds, R Muthusamy: Abnormal ventricular conduction following dothiepin overdose simulating acute myocardial infarction. Heart 2000;83:289.