Sindrome de Brugada: Reporte de un caso y revisión de la literatura.

Abstract

Desde su primera descripción el Sindrome de Brugada ha despertado gran interés científico como causa de muerte súbita. Presentamos el caso de un varón de 45 años quien ingresó al hospital en arresto cardiaco y en su evolución se le diagnosticó Sindrome de Brugada lográndose el implante de un cardiodesfibrilador como opción terapéutica definitiva. Resaltamos la importancia de reconocer el patrón electrocardiográfico característico y de considerar esta canalopatía en el diagnóstico diferencial de muerte súbita.

Cardioverter defibrillator placement in a young woman with Brugada syndrome: A case report and review

“…It is important to remember that the data found on the BS ECG can be unmasked or intensified by vagal stimulation. Neuro Cardiogenic Syncope (NCS) has been described in patients with BS and there is increasing evidence that autonomic dysfunction contributes significantly to arrhythmogenesis of the disease [20,21]; coupled with this, the existence of a total loss of the ordinary balance between the sympathetic and the parasympathetic cardiac function in the syndrome [4], this balance being the predisposition to the arrhythmias to cause a reduction in the sympathetic activity and the consequent predominance of the parasympathetic tone; partially explaining the higher incidence of ventricular arrhythmias and sudden death in rest and during sleep [1,4,17,21,22]. In contrast, it is posed that the episodes of symptomatic hypotension described in this case were due to a lack of dietetic indications, according to the recommendations of the treating cardiologist.…”

“…Diagnosis of Brugada syndrome is established when a characteristic repolarization pattern called Type 1 of BS or "coved" in at least 2 right precordial leads (V1 to V3) is observed, and less frequently in the inferior leads (DII, DIII and aVF), characterized by a prominent ST-segment elevation of convex morphology with J-point amplitude or ST segment elevation ≥2 mm, followed by a negative T-wave, associated with a complete or incomplete right bundle branch block (Figure 3A) [3,17,21]. Two other repolarization patterns, respectively called Type 2 BS or saddleback (elevation of point J ≥ 2 mm, ST segment elevation ≥1 mm concave morphology, followed by positive or biphasic T wave) and BS Type 3 (Concave or convex morphology, with ST segment elevation <1 mm) are considered to be suggestive (Figures 3B and 3C) [3,14,21]. Occasionally electrocardiographic alterations become evident when the position of the V1 and V2 electrodes is raised one or two intercostal spaces with or without the use of sodium channel blockers [12].…”

“…The development of a Type 1 ECG of BS during the test is a criterion for stopping it, as well as the appearance of a type 2 BS pattern with an ST segment elevation ≥5 mm, aQRS widening ≥130% of its initial value or the development of any arrhythmia. The pharmacological test is only considered positive when there is a conversion to the ECG pattern type 1 in at least 2 right precordial leads [3,21]. First-degree AVB is observed in about 50% of cases of SCR, especially when the SCN5A gene mutation is identified.…”