In Brugada syndrome, spontaneous type 1 pattern (coved ST elevation ≥2mm in V1–V2 with RBBB morphology) is sufficient for diagnosis. The predominant ion channel implicated is loss-of-function mutation in SCN5A. How does fever precipitate arrhythmia in Brugada syndrome?
- A Fever increases heart rate, reducing diastolic filling time
- B Fever increases potassium channel conductance
- C Hyperthermia accelerates inactivation of the mutant SCN5A sodium channel, unmask the electrophysiological abnormality ✓
- D Pyrexia causes catecholamine surge triggering EADs
Explanation
Brugada syndrome results from heterozygous loss-of-function mutations in SCN5A (Nav1.5 cardiac sodium channel) that reduce the inward sodium current (INa). Fever accelerates the temperature-dependent inactivation kinetics of the mutant (but not normal) Na channels, further reducing functional INa in the right ventricular outflow tract epicardium, unmasking or worsening the type 1 Brugada pattern and precipitating ventricular fibrillation. This explains why fever-related sudden cardiac death in young males may represent undiagnosed Brugada syndrome. Antipyretics are critical in these patients.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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