Brugada syndrome is a rare genetic disorder of the cardiac sodium channels associated with an increased risk of sudden cardiac death. It is characterized by an electrocardiogram (EKG) showing a right bundle branch block with an elevation in the ST segment. This condition is associated with mutations in several pathologic genes including the most notable mutation in the SCN5A gene, which encodes for a voltage-gated cardiac sodium channel. The Brugada pattern on EKG can be spontaneous but can also be induced by a variety of etiologies including fever, electrolyte abnormalities, increased vagal tone and drugs such as sodium channel blockers, calcium channel blockers, tricyclic antidepressants and alcohol. One uncommon cause of Brugada syndrome is hyperglycemia. Of particular importance in diabetic patients, hyperglycemia can induce chronic cardiovascular complications as well as acute cardiac events via the induction of the Brugada pattern on EKG. We present a case of a 21-year-old non-insulin compliant diabetic man presenting to the Emergency Department with diabetic ketoacidosis (DKA) who exhibits the Brugada pattern EKG prior to developing ventricular tachycardia followed by cardiac arrest. The patient's condition was induced by prolonged hyperglycemia in the setting of DKA with relatively mild electrolyte and pH abnormalities. Herein, this case is presented to highlight the Brugada pattern leading to cardiac arrest as a potential consequence of hyperglycemia and inform physicians on its incidence.
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http://dx.doi.org/10.22551/2021.31.0802.10181 | DOI Listing |
Pediatr Neurol
January 2025
Faculty of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain; Pediatrics Research Group, Institut de Recerca Sant Pau (IR-Sant Pau), Barcelona, Spain; Pediatric Neurology Unit, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Background: Dravet syndrome (DS) is a severe developmental and epileptic encephalopathy associated with loss-of-function variants in the SCN1A gene. Although predominantly expressed in the central nervous system, SCN1A is also expressed in the heart, suggesting a potential link between neuronal and cardiac channelopathies. Additionally, DS carries a high risk of sudden unexpected death in epilepsy (SUDEP).
View Article and Find Full Text PDFBackground: Placement of right precordial leads in higher intercostal spaces (EEP-ECG) improves the detection of Brugada Syndrome (BrS). Given the potential difficulty of lead placement and the transient nature of BrS ECG patterns, we developed a model to predict EEP-ECG from a standard 12‑lead ECG.
Objective: To create and validate a model that derives EEP-ECG leads from a standard 12‑lead ECG.
Biomedicines
December 2024
Clinical and Rehabilitation Cardiology Division, San Filippo Neri Hospital, 00135 Rome, Italy.
Brugada syndrome (BrS) is an inherited arrhythmogenic disorder characterized by distinct electrocardiographic patterns and an increased risk of sudden cardiac death due to ventricular arrhythmias. Effective management of BrS is essential, particularly for high-risk patients with recurrent arrhythmias. While implantable cardioverter-defibrillator (ICD) is effective in terminating life-threatening arrhythmias, it does not prevent arrhythmia onset and can lead to complications such as inappropriate shocks.
View Article and Find Full Text PDFJACC Case Rep
January 2025
Division of Cardiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Structural abnormalities within the right ventricular outflow tract (RVOT) can present similarly to Brugada syndrome. A 34-year-old woman with no medical history presented with polymorphic ventricular tachycardia/ventricular fibrillation cardiac arrest and initial electrocardiogram showed type I Brugada pattern. Cardiac magnetic resonance imaging revealed prominent tissue thickening at the RVOT with late gadolinium enhancement.
View Article and Find Full Text PDFHeart Rhythm
January 2025
Dante Pazzanese Institute of Cardiology, Department of Electrophysiology, São Paulo, Brazil.
Background: Brugada syndrome (BrS) is a genetic heart disease that predisposes individuals to ventricular arrhythmias and sudden cardiac death. Although implantable cardioverter-defibrillators (ICDs) and quinidine are primary treatments, recurrent BrS-triggered ventricular arrhythmias can persist. In this setting, epicardial substrate ablation has emerged as a promising alternative for symptomatic patients.
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