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Hyperkalemia-induced Brugada phenocopy: a systematic review of case reports
Asmaa Zakria Alnajjar1, Afnan Ismail Ibrahim2, Mohamed Ellebedy3
1Faculty of Medicine, Al-Azhar University, Gaza, Palestine. asmaaalnjjar246@gmail.com.
Background:
Hyperkalemia-induced Brugada phenocopy is a transient electrocardiographic pattern that mimics the features of Brugada syndrome but is triggered by an elevation in serum levels of potassium. The objective of conducting this systematic review of case reports on hyperkalemia-induced BrP was to combine cases and increase the understanding base driving the clinical practice.
Methods:
We conducted a literature search in PubMed, WOS, Cochrane, and Scopus up to July 2024 for case reports of BrP induced by hyperkalemia. We considered case reports of patients with hyperkalemia and Brugada-like changes on ECG that resolved with the correction of hyperkalemia for inclusion. Extracted data included patient demographics, clinical presentation, ECG findings, potassium levels, management, and the outcomes.
Results:
Thirty-one case reports fit our inclusion criteria. Their ages ranged from 12 to 89years, with 60% being male. Most of the patients presented with symptoms of hyperkalemia such as weakness, palpitations, and chest pain. The ECG changes were typical of BrP and included the coved-type ST-segment elevation in leads V1-V3. The potassium levels at presentation varied from 6.1mmol/L to 9.5 mmol/L. The management strategies principally involved correction of hyperkalemia using intravenous calcium, insulin with glucose, and diuretics. In all patients, normalization of the potassium level was associated with resolution of the Brugada-like ECG pattern.
Conclusion:
Systemic hyperkalemia may induce BrP, a condition frequently mimicked on the ECG by Brugada syndrome and which resolves by properly treating the hyperkalemia. Such awareness will facilitate the making of an accurate diagnosis and management of this condition, avoiding unnecessary interventions based on Brugada syndrome. Further studies should aim at explaining the underlying pathophysiological mechanisms and the legislation of diagnostic criteria for hyperkalemia-induced BrP.
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