Abstract
The Brugada syndrome is a form of cardiac arrhythmia, characterized by electrocardiographic ST-Segment elevation in right precordial leads that affect young male patient, predisposing to malignant ventricular arrhythmia and sudden cardiac deaths. The majority of the patients with Brugada syndrome remain asymptomatic, however, patient can present with symptom like syncope, palpitation and aborted sudden cardiac death. Several pathogenic genes have been identified as associated with the disease but SCN5A is most prevalent one. The Brugada syndrome is diagnosed by typically cove shaped ST-segment elevation of >2 mm in greater than one precordial lead V1 and V2, occurring spontaneously or after provocative drugs test with IV administration of class 1 antiarrhythmic drug such flecainide or Ajmaline. Risk stratification and the need for treatment depend on the patient symptom, electrocardiography, family history and electrophysiological study. The treatment by implantable cardioverter defibrillators, the only effective treatment to date is appropriate. Other treatment options included pharmacological therapy (Quinidine) and Radiofrequency ablation of ventricular ectopies. This brief review focuses on epidemiology of Brugada syndrome, Genetic basis, mechanism, clinical presentation, ECG changes, risk stratification, Diagnostic criteria and management.
Highlights
Brugada syndrome was initially described by Pedro and Joseph Brugada in 1992 [1]
Fever modulates the phenotype and the risk of arrhythmias by Figure 3. 12 leads Electrocardiogram (ECG) showing Brugada syndrome type-1 ECG pattern showed coved ST-Segment elevation > 2 mm is followed by negative T-Wave with little or no isoelectric separation in right precordial leads from V1 to V3 [9]
The following life style measures are recommended in patients with diagnosis of Brugada syndrome: 1) Avoidance of drugs that aggravates or induces ST-Segment elevation in right precordial leads [68]
Summary
Brugada syndrome is a rare cardiac arrhythmia characterized by electrocar-. Brugada syndrome is defined electrocardiographically by a characteristic patter including J-Point and ST-segment elevation of 2 mm or greater, followed by a negative T wave in the right precordial leads [1]. The typical arrhythmia of Brugada syndrome is polymorphic ventricular tachycardia which can potentially degenerate to ventricular fibrillation and high risk of sudden cardiac death, predominantly in younger male patient with structural normal heart [1]. Repetitive monomorphic ventricular tachycardia including ventricular flutter occurring in Brugada syndrome is potentially lethal events. Most patients with Brugada syndrome are diagnosed only after cardiac arrest [2]. The only proven effective strategy for preventing sudden cardiac death (SCD) in Brugada syndrome patient is the use of implantable cardioverter defibrillators
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