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Intermittent Brugada syndrome misdiagnosed as acute myocardial infarction and unmasked with propafenone
  1. I Akdemir,
  2. V Davutoglu,
  3. M Aksoy

  1. ilyasakdemir{at}

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A 40 year old man was admitted to the emergency department with chest and left shoulder pain for an hour. His admission ECG revealed 3–5 mm ST segment elevation on leads V1–3 and right bundle branch block (RBBB). His previous ECGs were normal. Acute myocardial infarction was diagnosed and thrombolytic treatment initiated. Six hours later, there was no ST segment elevation on leads V1–3 or RBBB on the ECG, and all cardiac enzymes were within normal limits. Echocardiography was normal. Coronary angiography revealed normal coronary arteries. All ECGs were reviewed and it was decided that the diagnosis of acute myocardial infarction was incorrect. Because of typical ECG findings, an intermittent form of Brugada syndrome was suspected. To confirm the diagnosis (and because of the absence of ajmaline, flecainide, and procainamide) a provocation test with propafenone was performed. The test proved strongly positive for the Brugada syndrome. ECGs of his four family members revealed similar electrocardiographic abnormalities.

While magnetic resonance imaging (MRI) of the heart was normal, MRI of the neck delineated cervical herniation, which might explain the patient's symptoms.

Brugada syndrome can present with a typical ECG but in some cases the patient can present with concealed or intermittent forms. In the presented case propafenone unmasked ST segment elevation in leads V1–3 and RBBB. The blocking of the sodium channels and β adrenoreceptors contribute to the unmasking effect of propafenone.

This case indicates that Brugada syndrome may be confused with AMI, and that propafenone is useful for unmasking the Brugada syndrome ECG pattern.

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Admission ECG revealed ST elevation and RBBB.

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ECG findings normalised six hours later.

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Unmasking effect of propafenone following the provacation test (20 minutes after).