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Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience.

Kharazi A, Emkanjoo Z, Alizadeh A, Nikoo MH, Jorat MV, Sadr-Ameli MA - Indian Pacing Electrophysiol J (2007)

Bottom Line: In 3 patients, spontaneous coved-type ECG was found at baseline.No significant difference was found between symptomatic and asymptomatic patients (p=NS).The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient.

View Article: PubMed Central - PubMed

Affiliation: Department of Pacemaker and Electrophysiology, Rajaie Cardiovascular Research and Medical Center, Tehran, IRAN.

ABSTRACT

Background: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increase risk of sudden cardiac death. Risk stratification for the life-threatening arrhythmic events in Brugada syndrome is not yet established. In the present study, we report our experience in patients with Brugada syndrome, following an ICD implantation.

Methods and results: A total of 12 patients (11 men, 1 woman) with a mean age of 46.5+/-11.8 were studied. At diagnosis, 7 patients had syncope of unknown origin, 2 patients were asymptomatic, 2 patients were survivors of cardiac arrest, and 1 had documented clinical VT requiring direct cardioversion for termination. Age was similar between the symptomatic and asymptomatic patients (46.6+/-13 vs. 46+/-2.8, respectively). Two patients reported a family history of sudden cardiac death. In 3 patients, spontaneous coved-type ECG was found at baseline. In 9 patients, a class I antiarrhythmic drug administration unmasked the characteristic type I ECG. In 4 patients (2 symptomatic with syncope at presentation and 2 asymptomatic), who underwent PES, sustained polymorphic VT or VF was induced. VF was induced by single extrastimuli in 2 symptomatic patients (1 from RV apex and 1 from RVOT). In 2 asymptomatic patients, VF was induced by two and triple ventricular extrastimli (1 from RV apex and 1 from RVOT). None of them experienced an event during follow-up. No significant difference was found between symptomatic and asymptomatic patients (p=NS). The mean follow-up period for the entire study population was 27.83+/-11.25 months. During follow-up, 2 patients (one with prior cardiac arrest and another with syncope) had VF. Both of them had a type I ECG after provocation with a class I antiarrhythmic drug. None of them had undergone programmed ventricular stimulation. Five patients (41.7 %) had inappropriate ICD interventions during follow-up. The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient.

Conclusion: Knowledge about Brugada syndrome is steadily progressing but there are still unanswered issues dealing with the risk stratification and the management of patients.

No MeSH data available.


Related in: MedlinePlus

Electrocardiographic recording of oversensing of T waveresulted in the misdiagnosis of sinus tachycardia as ventricular fibrillation
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Figure 2: Electrocardiographic recording of oversensing of T waveresulted in the misdiagnosis of sinus tachycardia as ventricular fibrillation

Mentions: Two patients had a family history of sudden cardiac death, but 3 patients had other family members with Brugada syndrome. The patient number 2 presented with frequent ICD (Marquis VR 7230, Medtronic Inc., Minneapolis, MN, USA) discharges, two years after implantation. Device interrogation revealed intermittent T wave oversensing due to changes in R:T ratio which could not be resolved by device reprogramming and required implantation of a new sense /pace lead in another position where an R wave of greater amplitude made oversensing less likely (Figure 2). In patient number 7, quinidine eliminated repetitive VF episodes, known as electrical storm. Therefore, quinidine was continued in combination with ICD. Neither syncope nor ventricular tachycardia occurred during the administration of quinidine.


Mid-term follow-up of patients with Brugada syndrome following a cardioverter defibrillator implantation: a single center experience.

Kharazi A, Emkanjoo Z, Alizadeh A, Nikoo MH, Jorat MV, Sadr-Ameli MA - Indian Pacing Electrophysiol J (2007)

Electrocardiographic recording of oversensing of T waveresulted in the misdiagnosis of sinus tachycardia as ventricular fibrillation
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1764907&req=5

Figure 2: Electrocardiographic recording of oversensing of T waveresulted in the misdiagnosis of sinus tachycardia as ventricular fibrillation
Mentions: Two patients had a family history of sudden cardiac death, but 3 patients had other family members with Brugada syndrome. The patient number 2 presented with frequent ICD (Marquis VR 7230, Medtronic Inc., Minneapolis, MN, USA) discharges, two years after implantation. Device interrogation revealed intermittent T wave oversensing due to changes in R:T ratio which could not be resolved by device reprogramming and required implantation of a new sense /pace lead in another position where an R wave of greater amplitude made oversensing less likely (Figure 2). In patient number 7, quinidine eliminated repetitive VF episodes, known as electrical storm. Therefore, quinidine was continued in combination with ICD. Neither syncope nor ventricular tachycardia occurred during the administration of quinidine.

Bottom Line: In 3 patients, spontaneous coved-type ECG was found at baseline.No significant difference was found between symptomatic and asymptomatic patients (p=NS).The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient.

View Article: PubMed Central - PubMed

Affiliation: Department of Pacemaker and Electrophysiology, Rajaie Cardiovascular Research and Medical Center, Tehran, IRAN.

ABSTRACT

Background: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increase risk of sudden cardiac death. Risk stratification for the life-threatening arrhythmic events in Brugada syndrome is not yet established. In the present study, we report our experience in patients with Brugada syndrome, following an ICD implantation.

Methods and results: A total of 12 patients (11 men, 1 woman) with a mean age of 46.5+/-11.8 were studied. At diagnosis, 7 patients had syncope of unknown origin, 2 patients were asymptomatic, 2 patients were survivors of cardiac arrest, and 1 had documented clinical VT requiring direct cardioversion for termination. Age was similar between the symptomatic and asymptomatic patients (46.6+/-13 vs. 46+/-2.8, respectively). Two patients reported a family history of sudden cardiac death. In 3 patients, spontaneous coved-type ECG was found at baseline. In 9 patients, a class I antiarrhythmic drug administration unmasked the characteristic type I ECG. In 4 patients (2 symptomatic with syncope at presentation and 2 asymptomatic), who underwent PES, sustained polymorphic VT or VF was induced. VF was induced by single extrastimuli in 2 symptomatic patients (1 from RV apex and 1 from RVOT). In 2 asymptomatic patients, VF was induced by two and triple ventricular extrastimli (1 from RV apex and 1 from RVOT). None of them experienced an event during follow-up. No significant difference was found between symptomatic and asymptomatic patients (p=NS). The mean follow-up period for the entire study population was 27.83+/-11.25 months. During follow-up, 2 patients (one with prior cardiac arrest and another with syncope) had VF. Both of them had a type I ECG after provocation with a class I antiarrhythmic drug. None of them had undergone programmed ventricular stimulation. Five patients (41.7 %) had inappropriate ICD interventions during follow-up. The cause of inappropriate therapy was sinus tachycardia in 2 patients, AF in 2 patients and T wave oversensing in 1 patient.

Conclusion: Knowledge about Brugada syndrome is steadily progressing but there are still unanswered issues dealing with the risk stratification and the management of patients.

No MeSH data available.


Related in: MedlinePlus