Brugada-type Electrocardiographic Pattern Research Articles

Patrón Brugada desenmascarado por fiebre…y algo más

Patrón Brugada desenmascarado por fiebre…y algo más

Long-Term Electrocardiographic Follow-up From Childhood of an Adult Patient With Brugada Syndrome Associated With Sick Sinus Syndrome A Case Report

We had the unique opportunity of following the electrocardiographic (ECG) course of a 13-year-old male with sinus dysfunction and atrial flutter who subsequently developed a Brugada-type ECG pattern associated with sick sinus syndrome at 25 years old. Family history showed that the patient's mother and maternal grandfather suddenly died while sleeping at night. When the patient was 13 years old, he lost consciousness after running a marathon. The patient was diagnosed with sinus dysfunction and atrial flutter, and he underwent pacemaker implantation at 15 years old. ECG examinations performed between 13 and 20 years old showed incomplete right bundle branch block and ST elevation with early depolarization. On ECG examinations performed when the patient was 21 years old and thereafter, the V(2) lead always showed a saddleback-type ST elevation. At 25 years old, the late potential was positive and the electrophysiological study induced ventricular fibrillation. A challenge test with pilsicainide showed remarkable ST elevation by the V(2) lead. The 24-h Holter ECG monitoring showed remarkable ST elevation after eating a snack and during night time when the patient was asleep. The patient was diagnosed with Brugada syndrome and an implantable cardioverter-defibrillator was implanted. Genetic analysis did not reveal mutation of the SCN5A gene.

Prevalence of Brugada sign in a Greek tertiary hospital population

The purpose of the present study was to determine for the first time the prevalence of Brugada-type electrocardiographic (ECG) pattern (Brugada sign) in unselected individuals served by an urban Greek tertiary hospital during a 4-year time period. Among 11,488 individuals (6640 males, 4848 females), 25 (23 males, 2 females, aged 36.8 +/- 19.2 years) were found to display the Brugada sign (0.22%). Two cases exhibited the diagnostic type 1 ECG pattern (0.02%) and 23 subjects fulfilled the ECG criteria for type 2 or 3 patterns (0.2%). The incidence of Brugada sign was higher among men (0.34%) than in women (0.04%). Structural heart disease was established in four cases (one of them exhibiting a type 1 ECG pattern). Twenty-one individuals (19 males, 2 females, aged 29.7 +/- 10.7 years) without structural heart disease displaying Brugada-type ECG features (4 cases with spontaneous or procainamide-induced type 1 ECG pattern) were subsequently selected and closely followed up for 24 +/- 12 months. No mortality or life-threatening ventricular arrhythmias were recorded during this period. The Brugada-type ECG pattern is infrequently seen in a Greek hospital-based population. All subjects with Brugada sign and structurally normal hearts displayed a benign clinical course without arrhythmic events during a relatively long follow-up period.

Three Elderly Cases with Brugada-type Electrocardiographic Pattern Unmasked by Pilsicainide at the Toxic Level

We describe three elderly patients with Brugada-type electrocardiographic abnormalities unmasked by a high plasma concentration of the Class IC antiarrhythmic drug pilsicainide, caused by renal dysfunction. The electrocardiograms showed right bundle branch block pattern and ST segment elevation in the precordial leads in patients 1 and 2, and a polymorphic wide QRS wave in patient 3. The serum concentrations of pilsicainide were 2.85, 2.50, and 4.18 microg/ml, which were much higher than the therapeutic range (0.16-0.24 microg/ml). Withdrawal of the drug reversed the electrocardiographic changes. Careful observation is necessary to avoid life-threatening arrhythmias whenever pilsicainide is administered to elderly patients.

1130-220 Brugada-type electrocardiographic pattern and ST-segment alternans in right precordial leads during percutaneous coronary intervention of the proximal right coronary artery

1130-220 Brugada-type electrocardiographic pattern and ST-segment alternans in right precordial leads during percutaneous coronary intervention of the proximal right coronary artery

Two-year case collection of the Brugada syndrome electrocardiogram pattern at a large teaching hospital.

Recommendations have recently emerged suggesting that the presence of the Brugada electrocardiographic (ECG) pattern in an otherwise asymptomatic individual warrants electrophysiologic testing for inducible ventricular arrhythmias. However, the prevalence of this pattern in the general population and its specificity for identifying those likely to develop the true Brugada syndrome are not known. The purpose of this study was to collect ECGs that displayed the Brugada pattern from unselected, noncardiac patients at a single institution to determine whether the implied prevalence in the literature may represent a significant underestimation of the true prevalence. We performed a prospective case collection of Brugada-patterned ECGs over a 2-year time period from unselected, noncardiac patients at a large urban teaching hospital. Of approximately 12,000 noncardiac patients, 52 were found to have an ECG pattern fully consistent with the Brugada sign. The Brugada type ECG pattern is much more prevalent than previously reported when rigorously searched for in a prospective manner. More data are needed on its specificity for predicting future arrhythmic events in asymptomatic individuals before recommendations are made for extensive evaluation in this group.

Brugada-Type Electrocardiographic Pattern Induced by Cocaine

Right bundle branch block with coved ST-segment elevation in leads V1 through V3 is the electrocardiographic (ECG) marker of the Brugada syndrome. We describe a healthy young man with a normal baseline ECG in whom a transient Brugada pattern was observed repeatedly after recreational cocaine use. Intravenous administration of procainamide and subsequent intravenous propranolol followed by noradrenaline failed to reproduce the Brugada sign. An electrophysiologic study performed in the presence of the Brugada ECG pattern showed no inducible arrhythmias. This case illustrates that, in susceptible individuals, cocaine may provoke the Brugada sign. The clinical importance of this cocaine-induced ECG abnormality is currently unknown.