Tachycardia-dependent Brugada phenocopy due to hyperkalemia

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A 73-year-old woman with history of ischemic heart disease and heart failure presented with shortness of breath and reduced urine output. She was taking aspirin, lisinopril, furosemide, carvedilol, and spironolactone. Her lab results revealed severe hyperkalemia at 7.2 mmol/L and acute kidney disease with a creatinine at 4.2 mg/dL (371 mmol/L).
Her initial ECG showed evidence of hyperkalemia (“peaked T-waves, widening of the QRS) with a distinctive type-1 Brugada ECG pattern (“coved”) when her heart rate temporarily increased from 87 to 125 bpm (Figure A, red arrow). After electrolyte correction and heart failure treatment, her ECG normalized (Figure B). A procainamide test was negative to reproduce a Brugada ECG pattern. This case represents a tachycardia-dependent Brugada phenocopy. Brugada phenocopies are clinical entities that present with an ECG pattern identical to congenital Brugada syndrome and may obey to various clinical conditions, including myocardial ischemia, electrolyte disturbances, anatomic variations, metabolic disorders and others.
A previous report has shown normalization of the Brugada ECG pattern following postextrasystolic pauses (phase 4). The presented case adds up to the understanding of the dynamicity of the ion channel dysfunction, which is not necessarily associated with genetic mutations.
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