ABC | Volume 110, Nº3, March 2018

Case Report Gil et al. Propafenone Intoxication Arq Bras Cardiol. 2018; 110(3):292-294 Figure 1 – ECG on admission from case 1. Figure 2 – ECG from second clinical case revealing type-1 Brugada pattern. gastrointestinal, hepatic and neurological (convulsions, amnesia, peripheral neuropathy and exacerbation of myasthenia) reactions. 2 A number of clinical signs and symptoms have been associatedwith propafenone intoxication, ranging from nausea and vomiting to seizures, coma, respiratory depression and cardiovascular collapse (Table 1). 4 Propafenone may be responsible for several ECG changes, including sinus bradycardia, sinus arrest, atrial fibrillation, prolongation of the PR interval, intraventricular conduction abnormalities (QRS and QT widening and right bundle branch block), Brugada pattern, 8-11 ventricular tachycardia, ventricular flutter or fibrillation and cardiac arrest. 1,4 The authors describe two cases of voluntary ingestion of excessive doses of propafenone, both with successful outcomes. There is no specific treatment. A timely gastric lavage was attempted in both cases. When performed promptly, gastric lavage is the only effective way of eliminating excessive doses of propafenone. 1,3 In both cases, tonic-clonic seizures were observed. This is an important neurological manifestation of propafenone intoxication. 3,4 The reason for seizure occurrence is uncertain. Saz et al. 3 and Clarot et al. 4 suggest that it may be attributed either to a direct toxic effect of propafenone or to cerebral hypoperfusion caused by arrhythmia or conduction disturbance. In the first case, all the major clinical warning signs were observed: cardiac failure, conduction disturbance, and seizures. 4 There was a progressive worsening of the neurological and respiratory status. The patient eventually became comatose, requiring mechanical ventilation. Cardiac failure was also observed, resulting in arterial hypotension, and requiring catecholaminergic support with positive inotropic and vasoconstrictive drugs. After progressive elimination of the drug, weaning from supportive measures was fairly straightforward. Another important aspect is the dynamic ECG changes. The patient underwent rhythm changes (going from sinus arrhythmia to atrial fibrillation and finally returning to normal sinus rhythm) and intraventricular conduction disorders (with widening of the QRS interval and enhancement of the RBBB pattern). These changes occurred only in the first 3 hours after admission, corresponding to peak serum concentration. 4 This highlights the importance of close monitoring and prompt treatment in the first hours following propafenone overdose. In the second case, the ingestion of supratherapeutic levels of propafenone revealed a Brugada type 1 pattern on surface ECG. Concealed or intermittent forms of the Brugada Syndrome have been described in a few subset of patients, namely following hyperventilation, beta-adrenergic blockade and alpha-adrenergic stimulation, muscarinic receptors stimulation, and sodium channels blockade inducing or increasing ST elevation. 10,11 In this particular case, propafenone is able to unmask the concealed Brugada phenomenon due to its sodium channel and beta‑adrenergic blocking activity. 10 The appearance of the Brugada pattern in response to type IC antiarrhythmic drugs does not seem to be associated with a great risk for polymorphic arrhythmias; however, further investigation is needed. 11 In this case, the Brugada pattern disappeared after drug elimination. Both patients were closely monitored for 36 to 48 hours. The propafenone elimination half-time ranges from 17 ± 8 hours for poor metabolizers to 5±2 hours for extensive metabolizers, 1,4 thus monitoring over that period of time is 293