Chameleons

Nable, Jose V.; Lawner, Benjamin J.

doi:10.1016/j.emc.2015.04.004

Cited by 7 publications

(1 citation statement)

References 36 publications

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“…These STEMI mimics are caused by non-acute coronary syndrome conditions, including Brugada syndrome [ 8 ]. More common clinically-encountered conditions include: electrolyte abnormalities (ie, hyperkalemia, hypokalemia, hypercalcemia), shock (cardioversion/defibrillation), inflammation (myocarditis/ pericarditis), medications (ie, cardiac, chemotherapeutics, psychotropics), toxins (ie, cocaine, amphetamines, ethanol), and mechanical cardiac and thoracic disorders (ie, aortic dissection, coronary aneurysm, pulmonary embolism) [ 7 – 10 ]. Conversely, certain underlying chronic conditions, including early repolarization, left bundle branch block, and left ventricular hypertrophy, can make the diagnosis of STEMI difficult, these are described as STEMI confounders , and also mimickers of OMI [ 7 ].…”

Section: Discussionmentioning

confidence: 99%

Brugada Pattern Manifesting During Hyperkalemia, Diabetic Ketoacidosis, and Acute Alcohol Intoxication

et al. 2021

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Patient: Male, 28-year-old Final Diagnosis: Alcohol intoxication • Brugada pattern • diabetic ketoacidosis • hyperkalemia Symptoms: Encephalopathy Medication:— Clinical Procedure: — Specialty: Cardiology Objective: Rare disease Background: Brugada syndrome is a rare ion channelopathy that can lead to sudden cardiac death and lethal arrhythmias in patients without a structural cardiac defect, the most common of which being the gain-of-function mutation of the SCN5a sodium ion channel involving phase 0 of the cardiac action potential. In 2012, BrS electrocardiogram findings were redefined and classified as either congenital Brugada syndrome (BrS) or Brugada pheno-copies (BrP). Several etiologies of BrP have been reported, such as metabolic derangements, electrolyte abnormalities, cardiovascular diseases, and pulmonary embolism. Case Report: A 28-year-old man presented to the Emergency Department unresponsive. An initial ECG taken by Emergency Medical Services (EMS) was interpreted as a STEMI. An initial ECG in the ED showed a Brugada type I ECG pattern in leads V1-V2 and hyperacute T wave abnormalities, among other findings. Additionally, the patient had a serum potassium level of 9 mmol/L, glucose level of 1375 mmol/L, and peak cardiac troponin-I of 20.452 μg/L. All underlying medical conditions were stabilized, electrolyte and metabolic abnormalities were corrected, and subsequent normalization of electrocardiographic findings was achieved. Conclusions: Distinguishing congenital Brugada syndrome from Brugada phenocopies can be difficult, especially when patients present to the ED with severe underlying conditions. Several factors can be used to direct clinical suspicion towards one or the other; however, confirmation may require EP studies and further tests. In this case, the following findings were suggestive of BrP: presence of an identifiable underlying abnormality, correction of the underlying condition resolves the ECG pattern, and the absence of family history of sudden cardiac death.

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