A 32-year-old man with no past medical or family history of note, presented with non-exertional syncope preceded by palpitations. He reported multiple similar episodes over a two-year period which had not been investigated. Baseline electrocardiography demonstrated typical atrial flutter with variable block, widened QRS (140ms) with a dominant R wave in V1 in conjunction with ≥2 mm ST segment elevation in V2 (saddle-back) and V3 (horizontal) without reciprocal changes. This pattern was highly suggestive of a channelopathy, in particular Brugada. He had inpatient cardiac monitoring which showed no change in his rhythm. Transthoracic echocardiogram revealed a normal left and right ventricular size and function, and cardiac MRI was normal including the absence of late gadolinium uptake. He was discharged with an implantable loop recorder, metoprolol and rivaroxaban. Four weeks later he represented with a further collapse. Interrogation of his device revealed atrial flutter with 1:1 conduction degenerating to ventricular tachycardia followed by ventricular fibrillation then asystole (for 15 seconds), before self-reverting to the original atrial flutter. An internal cardiac defibrillator was inserted. Two weeks post ICD insertion, he received an ICD discharge. Interrogation of the device again demonstrated 1:1 flutter degenerating into VT. Subsequently he was commenced on sotalol. He has been referred to a cardiac genetic clinic for primary arrhythmogenic screening and first-degree family members are being screened. Conclusions: We describe electrocardiogram findings in a young male with recurrent syncope and significant repolarisation abnormalities. He has had no further atrial flutter nor syncopal episodes since starting sotalol.