Syncope in Brugada syndrome patients: Prevalence, characteristics, and outcome

Sacher, Frédéric; Arsac, Florence; Wilton, Stephen B.; Derval, Nicolas; Denis, Arnaud; Guillebon, Maxime De; Ramoul, Khaled; Bordachar, Pierre; Ritter, Philippe; Hocini, Mélèze; Clémenty, Jacques; Jaı̈s, Pierre; Haı̈ssaguerre, Michel

doi:10.1016/j.hrthm.2012.04.013

Cited by 86 publications

(58 citation statements)

References 11 publications

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“…Such findings might suggest a slightly different arrhythmic risk in these 3 groups of patients. More importantly and in agreement with others, 29 we found that the mechanism of syncope in our 12 patients who exhibited recurrent syncope was likely vasovagal or nonarrhythmic.…”

Section: Syncopesupporting

confidence: 93%

Management of Brugada Syndrome

Belhassen

Rahkovich

Michowitz

et al. 2015

Circ: Arrhythmia and Electrophysiology

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Background-Information on long-term clinical outcome of patients with Brugada syndrome treated with electrophysiologically guided class 1A antiarrhythmic drugs (AAD) is limited. Methods and Results-An aggressive protocol of programmed ventricular stimulation was performed in 96 patients with Brugada syndrome (88% males; mean age, 39.8±15.9 years). Ten patients were cardiac arrest survivors, 27 had presented with syncope, and 59 were asymptomatic. Ventricular fibrillation was induced in 66 patients, including 100%, 74%, and 61% of patients with cardiac arrest, syncope, and no symptoms, respectively. All but 6 of the 66 patients with inducible ventricular fibrillation underwent electrophysiological testing on quinidine (n=54), disopyramide (n=2), or both (n=4). Fifty-four (90%) patients were electrophysiological responders to >1 AAD with similar efficacy rates (≈90%) in all patients groups. Patients with no inducible ventricular fibrillation at baseline were left on no therapy. After a mean follow-up of 113.3±71.5 months, 92 patients were alive, whereas 4 died from noncardiac causes. No arrhythmic event occurred during class 1A AAD therapy in any of electrophysiological drug responders and in patients with no baseline inducible ventricular fibrillation. Arrhythmic events occurred in only 2 cardiac arrest survivors treated with implantable cardioverter-defibrillator alone but did not recur on quinidine. All cases of recurrent syncope (n=12) were attributed to a vasovagal (n=10) or nonarrhythmic mechanism (n=2). Class 1A AAD therapy resulted in 38% incidence of side effects that resolved after drug discontinuation. Conclusions-Our data suggest that electrophysiologically guided class 1A AAD treatment has a place in our therapeutic armamentarium for all types of patients with Brugada syndrome. (Circ Arrhythm Electrophysiol.

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Section: Syncopesupporting

confidence: 93%

Management of Brugada Syndrome

Belhassen

Rahkovich

Michowitz

et al. 2015

Circ: Arrhythmia and Electrophysiology

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“…ICD indicates implantable cardioverter-defibrillator. 12 4 of 23 BrS patients with ICD implantation for suspected arrhythmic syncope subsequently developed recurrent syncope without arrhythmia on the ICD log. In a BrS patient with syncope for whom the clinical history is not typical of an arrhythmic origin, an implantable loop recorder may be helpful.…”

Section: Discussionmentioning

confidence: 99%

Outcome After Implantation of a Cardioverter-Defibrillator in Patients With Brugada Syndrome

et al. 2013

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Background-Implantable cardioverter-defibrillator indications in Brugada syndrome remain controversial, especially in asymptomatic patients. Previous outcome data are limited by relatively small numbers of patients or short follow-up durations. We report the outcome of patients with Brugada syndrome implanted with an implantable cardioverterdefibrillator in a large multicenter registry. Methods and Results-A total of 378 patients (310 male; age, 46±13 years) with a type 1 Brugada ECG pattern implanted with an implantable cardioverter-defibrillator (31 for aborted sudden cardiac arrest, 181 for syncope, and 166 asymptomatic) were included. Fifteen patients (4%) were lost to follow-up. During a mean follow-up of 77±42 months, 7 patients (2%) died (1 as a result of an inappropriate shock), and 46 patients (12%) had appropriate device therapy (5±5 shocks per patient). Appropriate device therapy rates at 10 years were 48% for patients whose implantable cardioverter-defibrillator indication was aborted sudden cardiac arrest, 19% for those whose indication was syncope, and 12% for the patients who were asymptomatic at implantation. At 10 years, rates of inappropriate shock and lead failure were 37% and 29%, respectively. Inappropriate shock occurred in 91 patients (24%; 4±4 shocks per patient) because of lead failure (n=38), supraventricular tachycardia (n=20), T-wave oversensing (n=14), or sinus tachycardia (n=12). Importantly, introduction of remote monitoring, programming a high single ventricular fibrillation zone (>210-220 bpm), and a long detection time were associated with a reduced risk of inappropriate shock. Conclusions-Appropriate therapies are more prevalent in symptomatic Brugada syndrome patients but are not insignificant in asymptomatic patients (1%/y). Optimal implantable cardioverter-defibrillator programming and follow-up dramati cally reduce inappropriate shock. However, lead failure remains a major problem in this population.

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“…18 None of the patients presenting with presumed nonarrhythmic or doubtful syncope experienced cardiac arrest during a 65-month follow-up period. In contrast, in the group presenting with suspected arrhythmic syncope (all of which received an implantable cardioverter-defibrillator) 5% subsequently developed spontaneous VF.…”

Section: Symptomsmentioning

confidence: 94%