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Response by Viskin to Letter Regarding Article, "Radiofrequency Ablation of Asymptomatic Brugada Syndrome: Don't Go Burning My Heart".

Circulation. 2018;138:2584–2585. DOI: 10.1161/CIRCULATIONAHA.118.036942 2584 In Response: Dr Aloia implies in his letter that my essay, “Don’t Go Burning My Heart,”1 represents an indiscriminate opposition to ablative procedures that precludes the possibility of having an extra tool in our fight against arrhythmic death. I beg to disagree. In fact, what I stated1 was that radiofrequency ablation of the epicardial arrhythmogenic substrate, as originally performed by Nademanee in patients with Brugada syndrome experiencing multiple episodes of spontaneous ventricular fibrillation (VF), represents an important landmark (published 7 years ago in Circulation) in the very same fight against arrhythmic death. One could promote radiofrequency ablation in patients with Brugada syndrome after a single episode of VF, considering that as many as 1 in 4 such patients may eventually develop an arrhythmic storm if left untreated. Ideally, this should be done in the setting of a randomized trial comparing radiofrequency ablation with no therapy (with implantable cardioverter-defibrillator backup) or comparing radiofrequency ablation with quinidine therapy. However, in the Italian study2 alluded to by Dr Aloia, only 29% of patients undergoing epicardial ablation belonged to that category. For this particular subgroup of patients, Dr Aloia emphasizes that the percentage of patients receiving appropriate therapy was 69.2% before the ablation but only 5.1% after the procedure. Dr Aloia fails to mention that for that comparison to be meaningful, the time at risk before and time after the procedure should be of comparable duration. However, this is probably not the case: The follow-up period between the time of the index arrhythmia and the ablation procedure, although not stated in the original article,2 was conceivably much longer than the median follow-up of 10 months (range, 3–13 months) after the ablation. The real issue at hand, however, is whether we have reached the point in time when patients with asymptomatic Brugada syndrome should be referred for epicardial ablation. The answer to that question, in my mind, is clearly negative. In particular, we should strongly discourage the performance of epicardial ablation of asymptomatic patients when their diagnosis of Brugada syndrome was made only recently or with a drug challenge. As predicted a decade ago,3 patients with Brugada syndrome diagnosed during the last 10 years have a more benign profile than those diagnosed previously. Specifically, their risk of developing spontaneous VF is lower, even if they have inducible VF.4 As explained before,1 the same holds true for patients who have only a type I Brugada pattern provoked by drugs. Dr Siena is correct when he states that our methods for risk stratification of patients with Brugada syndrome are imperfect; however, that is not a reason for indiscriminate epicardial ablation of asymptomatic individuals. After all, the main reason for the poor positive predictive value of our tests is the low rate of spontaneous VF in patients who are asymptomatic at the time of diagnosis. That is also the main reason for the poor performance of implanted defibrillators, in terms of risk versus benefit and in comparison with other channelopathies, when implanted in patients with asymptomatic Brugada syndrome.5 © 2018 American Heart Association, Inc. RESPONSE TO LETTER TO THE EDITOR