Electrophysiologically guided class 1A antiarrhythmic drug therapy resulted in 0 arrhythmic events over a mean follow-up of 113.3 months among electrophysiological drug responders.
Cohort (n=96)
Does electrophysiologically guided class 1A antiarrhythmic drug therapy prevent arrhythmic events in patients with Brugada syndrome?
Electrophysiologically guided class 1A antiarrhythmic drug therapy is highly effective in preventing arrhythmic events in patients with Brugada syndrome, though limited by a 38% rate of reversible side effects.
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.
Belhassen et al. (Thu,) conducted a cohort in Brugada syndrome (n=96). Electrophysiologically guided class 1A antiarrhythmic drugs (quinidine, disopyramide) vs. No therapy (for non-inducible VF) or ICD alone was evaluated on Arrhythmic events. Electrophysiologically guided class 1A antiarrhythmic drug therapy resulted in 0 arrhythmic events over a mean follow-up of 113.3 months among electrophysiological drug responders.