Visual Diagnosis in Emergency Medicine: Brugada-Pattern EKG in a Febrile Patient

Peter Ott
Case Report
A 27-year-old Navajo woman presented to an outside clinic with several days of high fevers and a sore throat. She denied chest pain, shortness of breath, palpitations and syncope. She had no past medical history, was not taking any medication or illicit drugs, and had an unremarkable family history. Her physical examination revealed an elevated temperature of 39.6°C (103.4°F), sinus tachycardia (110 beats/min), a blood pressure of 100/75 mm Hg, and intense pharyngeal erythema. The remainder of her examination and, in particular, her cardiopulmonary examination, was normal. Her laboratory tests showed a mild leucocytosis but normal values for sodium, potassium, calcium, magnesium, and troponin. She was diagnosed with a viral pharyngitis, admitted for observation and treated with supportive care with half normal saline as well as anti-pyretic therapy with acetaminophen 650 mg every 6 h. A routine 12-lead electrocardiogram (EKG) (Figure 1), taken while her oral temperature was 39.6°C (103.4°F), was abnormal. A 12-lead EKG (Figure 2) 2 days later, and with her oral temperature at 37.0°C (98.2°F), was normal. A cardiac echocardiogram showed no evidence of structural heart disease.

Discussion
The Brugada Syndrome is diagnosed in patients presenting with syncope or resuscitated sudden death and a characteristic 12-lead EKG pattern: coved ST-segment elevation (≥ 2 mm) and T wave inversion in the at least two pre-cordial leads (V1-V3).[1] Electrocardiographic variants, such as coved ST-segment elevation of < 1 mm, or saddle-shaped ST-segment elevation have also been reported. These patients typically have no evidence of structural heart disease.
The EKG changes are caused by alterations in the cardiac action potential due to a genetic defect in the cardiac sodium channel function. These action potential changes are believed to be more pronounced in the right ventricular epicardial region, leading to a transmural voltage gradient and thus to regional ST-segment elevation, which may predispose susceptible patients to ventricular tachycardia or fibrillation.[2] Symptomatic patients with the Brugada Syndrome are treated with the implantable defibrillator. The treatment of asymptomatic patients is less defined.
Our patient's initial EKG, taken while febrile, showed: coved ST-segment elevation of 3-4 mm and T wave inversion in two pre-cordial leads (V1 and V2).
Of interest and relevant to this case, recent studies have shown that certain gene mutations of the sodium channel, capable of producing these EKG changes, are sensitive to temperature, displaying altered channel function only at elevated temperature.[3] Our patient displayed typical Brugada EKG changes only during her febrile state, suggesting that she may indeed carry such a temperature-sensitive gene.
Brugada-type EKG changes and ventricular dysrhythmias occurring only during a febrile illness have been reported by others.[4,5] Therefore, prompt therapy of any febrile illness seemed appropriate for our patient. She was not referred for defibrillator implantation. Screening of family members was recommended. The occurrence of (near)syncope or palpitations in a febrile patient should prompt an EKG and heart rhythm monitoring.
References
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Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST segment elevation. Circulation. 1999; 100:1660-1666.
Dumaine R, Towbin JA, Brugada P, et al.. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada Syndrome are temperature dependent. Circ Res. 1999; 85:803-809.
Porres JM, Brugada J, Urbistondo V, Garcia F, Reviejo K, Marco P. Fever unmasking the Brugada syndrome. Pacing Clin Electrophysiol. 2002; 25:1646-1648.
Saura D, Garcia-Alberola A, Carillo P, Pascual D, Sanchez JM, Valdes M. Brugada like electrocardiographic pattern induced by fever. Pacing Clin Electrophysiol. 2002; 25:856-859.