What is the Diagnosis?

A female 82-year-old Caucasian patient with a history of paroxysmal atrial fibrillation (AF) for several years, with palpitation crises of varying duration between a few minutes and several hours, without clinical control, using beta-blockers and diltiazem. The patient presented complaints of fatigue on moderate efforts, without precordial pain or syncope, with progressive asthenia and indisposition. She informed three previous hospitalizations for chemical cardioversion of AF.


8/8 hours), without control of palpitations and with feeling of discomfort and weakness.
On physical examination, the patient was in good general condition, with no signifi cant abnormalities. Her blood pressure was at 135/80 mmHg, with a heart rate of 72 bpm, irregular rhythm due to the presence of extrasystoles, normophonetic sounds in two times and mild systolic murmur at a mitral focus.
Laboratory tests were within normal limits. Th e patient presented Doppler echocardiography with left ventricle (LV) with standard segmental dimensions and contractility, ejection fraction of 68%, slight concentric LV hypertrophy, left atrium with slight increase (44 mm), alteration in LV distensibility, presence of mild mitral valve insuffi ciency and absence of pulmonary arterial hypertension or dilatation of right chambers. A 24-hour Holter performed one month before the examination showed the presence of sinus rhythm, mimic frequency of 49, maximum of 86, with a mean of 64 bpm, presence of rare atrial ectopias (29 isolated, 1 episode of atrial tachycardia with 5 beats and atrial frequency of 108 bpm), rare ventricular ectopias (78 isolated, without pairs or ventricular tachycardias) with fi rst-degree AV block during sleep, QRS with duration at the maximum limit of normality (0.12 s) and nonischemic changes of ventricular repolarization.
Her electrocardiogram (Figure 1) showed the presence of sinus rhythm, mild interatrial conduction disorder (P wave duration of 125 ms), AV interval at the upper limit of normality (0.20 s), QRS with 125 ms duration and presence of isolated ventricular extrasystoles. Th e presence of alterations in ventricular repolarization, with ST-segment elevation in V1 and V2 derivations, with descending "saddle-back" concavity, and T waves inversion drew considerable attention.
Th ese alterations seemed very suggestive of the corresponding pattern of Brugada syndrome (SBr).
On this occasion, we opted for the suspension of propafenone and the introduction of amiodarone. Th is decision was based both on the ineffi ciency of the drug in controlling AF crises and on the interpretation that propafenone could have some role in the electrocardiographic pattern of SBr (see discussion below). Also, the prevention of thromboembolic accidents was optimized, with the replacement of clopidogrel by oral anticoagulants. Th e patient did not accept the suggestion of treating AF by catheter ablation.
Fifteen days after changing the antiarrhythmic medication, the patient returned to the clinic, and a new electrocardiogram was performed, shown in Fig. 2, with an evident disappearance of the SBr pattern.
Th e patient presented signifi cant clinical improvement, remaining for more than two years without clinical recurrence of AF, with control by serial Holter without signifi cant changes, keeping the electrocardiographic pattern free of the SBr pattern.  Some authors discuss the clinical importance of "drug-induced SBr", with interpretations that these cases represent "phenocopy" of the clinical pattern of spontaneous SBr type 1, that is, the drug-induced electrocardiographic manifestation did not have the same clinical significance. However, most authors prefer to be cautious until the real clinical role of these cases is defined, preferring the term "drug-induced SBr" [3][4][5][6] . There are reports that after an aborted cardiac arrest, both the presence of spontaneous and drug-induced SBr may have similar clinical meanings 7 .
The practical importance of understanding the so-called "drug-induced SBr" is that many patients with channelopathies such as SBr (manifest or latent), short QT syndrome, J wave syndrome, among others, may develop it with atrial fibrillation and be treated with propafenone, manifesting an increased risk of potentially severe ventricular arrhythmias 6,8 . There is still no consensus if all manifestations of "drug-induced SBr" present the same prognostic significance, with reports that different drugs at different doses may present different risks of development of ventricular arrhythmias 9 .

ANSWER
Currently, we believe that patients with a clinical or electrocardiographic pattern compatible with SBr should be investigated about the possible use of medication that may be responsible for the condition and, if this information is positive, suspend the use of such drug. This was the case with the patient analyzed in this article, diagnosed as "drug-induced SBr", which was reversed after the suspension of propafenone.