Patrice Wendling

June 16, 2016

NICE, FRANCE ( updated ) — Epicardial ablation normalized ECG patterns in 100% of symptomatic and asymptomatic patients with Brugada syndrome in what was described as the largest study to date[1].

Only two of the 75 consecutive patients showed a questionable ECG pattern 1 week after ablation and underwent successful repeat ablation 3 months later.

After 3 to 20 months of follow-up, no patients showed phenotypic manifestations of Brugada, nor was ventricular tachycardia (VT)/ventricular fibrillation (VF) inducible.

The results "open up a new era" for patients with Brugada syndrome, particularly those in the gray zone who don't meet current recommendations for implantable cardioverter-defibrillator (ICD) therapy because they have very few symptoms or refuse ICD implantation. "I think we can offer a different option, and that option can be ablation," principal investigator Dr Carlo Pappone (University of Milan, Italy) said in a late-breaking EP session at the European Heart Rhythm Association (EHRA) EUROPACE-CARDIOSTIM 2016 meeting.

He said a multicenter randomized trial is necessary to demonstrate superiority over ICD therapy but described epicardial ablation guided by flecainide infusion as a definitive treatment.

Pappone told heartwire from Medscape, "In our series, all symptomatic patients with [the] worst clinical presentation had no recurrences, and stable persistent ECG normalization suggests that regardless of the symptoms, epicardial ablation of the substrate may be considered as a potential cure for Brugada syndrome."

The ongoing prospective registry study now has 110 patients, and none have had ECG abnormality or VT/VF inducibility with a median follow-up of 6 months (maximum 22 months), but it will require longer follow-up, he said. "Another limitation is that these results have been obtained from a single high-volume experienced center and do not automatically apply to other lower-volume centers, which could have more complications and perhaps not as high a success rate."

Dr Sami Viskin (Tel Aviv University, Israel) told heartwire that radiofrequency ablation of the outflow tract may now be seen as a potentially lifesaving procedure for the small percentage of patients with Brugada syndrome with severe arrhythmic manifestations who are intolerant to drug therapy. However, "one could definitely argue that it is too early to recommend epicardial radiofrequency ablation to asymptomatic patients."

He noted that the Italian lay press is already proposing ablation as "the cure for Brugada syndrome," but the vast majority of asymptomatic patients discovered incidentally will remain asymptomatic all their life even in the absence of therapy. The risk of cardiac arrest in these patients is estimated at less than 1% per year, but by how much less is not really known, because this widely quoted number uses appropriate ICD shocks as a surrogate for cardiac arrest—a measure that has been shown to overestimate the true number of patients that would have died without an implanted device.

Viskin said the current series expands on a prior report by Nademanee et al[2], in which ablation allowed nine Brugada patients with two to six episodes of ventricular arrhythmia per month to remain completely free of arrhythmias (in the absence of antiarrhythmic drugs in all but one case) for 2 years after ablation. However, only a handful of patients in the current series had a history of cardiac arrest, whereas 38% had dizziness or syncope as their worst symptomatic manifestation.

Prospective Registry

The analysis included 41 symptomatic and 34 asymptomatic patients, of whom 18 had a family history of sudden death, six had previous aborted sudden death, 17 had a spontaneous type 1 ECG, and 72 patients were VT/VF inducible. Nine patients had arrhythmic storms at baseline. Epicardial voltage, local activation, and duration maps were all assessed by color-coded maps using the CARTO3 system (Biosense Webster).

Through a series of cases, Pappone highlighted the effect of flecainide infusion before ablation to "unmask" prolonged and fragmented potentials in the right ventricular outflow tract (RVOT) and right ventricular free wall area.

Epicardial mapping revealed a concentric "onionlike" distribution surrounded by normal healthy tissue and a pattern in which the wider the low-voltage area, the higher the ST-segment elevation.

"Overall, voltage and activation maps before and after flecainide did not show significant abnormalities. Only duration maps were able to identify abnormal areas of prolonged fragmented or delayed potentials, which increased in size after flecainide in all patients," he said.

Areas with fragmented signals increased after flecainide from 4.9 cm2 to 20.9 cm2 for potentials >200 ms, from 0.7 cm2 to 9.1 cm2 for potentials >250 ms, and from 0.2 cm2 to 3.3 cm2 for potentials >280 ms.

Low-voltage areas (<1.5 mV) and mean duration of local abnormal ventricular electrograms also increased after flecainide from 2.3 cm2 to 8.1 cm2 and from 161.5 ms to 231.4 ms, respectively.

After the procedure, two patients had pericarditis that resolved with nonsteroidal anti-inflammatory drugs. Two other patients experienced pericardial effusion during follow-up that required pericardiocentesis.

Time cut short a discussion of the results save for one question on how this technique should fit into clinical practice. Dr Pappone responded, "We are ablating the general population of Brugada-syndrome patients. We are not concentrating our interests on the very symptomatic patient with [arrhythmic] storm."

Viskin commented that while no procedural complications were reported in the series, the list of things that can go wrong while ablating the epicardial aspect of the heart "is not inconsequential." Also, physicians have learned from ablation procedures for atrial fibrillation that the scars created with the ablation may cure the original arrhythmia while facilitating the onset of new monomorphic arrhythmias never observed before the procedure. Similarly, the scar created in the right ventricle during corrective surgery for congenital abnormalities is a well-documented source of monomorphic ventricular tachycardia, but only years after the original intervention. "Therefore, the long-term effects of this new procedure ought to be better understood before it is widely recommended as a standard therapy for asymptomatic patients."

Pappone and Viskin reported no relevant financial relationships.

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