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A 52 year old white man presented having woken up feeling dizzy and unwell. He went to the bathroom and on returning to his bedroom he lost consciousness. He came around spontaneously with no evidence of neurological deficit. He did not have any palpitations. His initial electrocardiogram (ECG) showed 2 mm ST elevation in V2 only (fig 1). The ST elevation in the right side of the precordial leads was associated with a partial right bundle branch block pattern and varied spontaneously over time. There was no evidence of an acute coronary syndrome. We then performed an intravenous flecainide challenge. His baseline ECG showed minor concave ST elevation in V2 only but then he went on to develop classical Brugada changes with a maximum of 5 mm ST elevation in V2 associated with T wave inversion (fig 2). No arrhythmia was provoked. Coronary angiography was normal and he was fitted with an implantable cardiodefibrillator. Brugada syndrome is characterised by marked ST-segment elevation in the right precordial ECG leads (unrelated to ischaemia, electrolyte abnormalities, or structural heart disease) with a morphology of the QRS complex resembling a right bundle branch block, and is associated with a high risk for sudden death.1
The mechanisms responsible for the electrocardiographic actions of class I antiarrhythmic agents in Brugada syndrome are thought to be due to their ability to block sodium channels.2 Strong sodium channel blockade facilitates the loss of the right ventricular epicardial plateau phase by altering the balance of current at the end of phase 1 of the action potential from inward to outward. The result is an all or nothing repolarisation of the right ventricular action potential and marked abbreviation of the epicardial action potential duration. The loss of the plateau in right ventricular epicardium but not endocardium creates a transmural voltage gradient that manifests as an ST-segment elevation in the right precordial leads of the ECG.
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