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This corrects the article: “Ioannou A. Evolution of Disease-modifying Therapy for Transthyretin Cardiac Amyloidosis. Heart International. 2024;18(1):30-37”. Two typography errors were included incorrectly due to an editorial error. In Table 1, “eplontersen” was incorrectly written as “eplomtersen”. This has been corrected in the text. In the section “Eplontersen”, the administration schedule should be written as […]

81/The role of 24-hour ambulatory 12-lead ECG in risk stratification in Brugada syndrome

R Williams (Presenting Author) - Royal Papworth Hospital, Cambridge, UK; K Divulwewa - Royal Papworth Hospital, Cambridge, UK; C Martin - Royal Papworth Hospital, Cambridge, UK; M Virdee - Royal Papworth Hospital, Cambridge, UK; S Agarwal - Royal Papworth Hospital, Cambridge, UK; D Begley - Royal Papworth Hospital, Cambridge, UK; P Heck - Royal Papworth Hospital, Cambridge, UK; S Fynn - Royal Papworth Hospital, Cambridge, UK; A Grace - Royal Papworth Hospital, Cambridge, UK; G Mellor - Royal Papworth Hospital, Cambridge, UK
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Published Online: Oct 3rd 2008 European Journal of Arrhythmia & Electrophysiology. 2019;5(Suppl. 1):abstr81
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Background: The presence of a spontaneous type 1 Brugada ECG pattern and previous syncope or cardiac arrest have consistently been associated with increased risk of sudden cardiac death (SCD) in Brugada Syndrome (BrS). In contrast asymptomatic individuals with a drug-induced type 1 pattern are at low risk. However, the ECG phenotype is known to be highly dynamic. We hypothesised ambulatory 12-lead ECG may be superior to ajmaline provocation for identifying patients with BrS and a moderate-to-high risk of arrhythmic events.

Methods: Patients with a previously documented type 1 Brugada ECG pattern (spontaneous, fever- or ajmaline-induced) underwent 12-lead 24-hour ambulatory ECG monitoring with modified high RV leads. Patients were classified as either ‘≥ Moderate Risk (previous spontaneous type 1 ECG pattern or previous arrhythmic syncope/cardiac arrest) or ‘Low Risk’ (Asymptomatic and a drug-induced ECG pattern only). The presence of Brugada ECG patterns and J-point amplitude (irrespective of ECG morphology) were recorded at 30 min intervals throughout 24 hours. The 24-hour ‘Type 1 burden’ was calculated as time present (hours) x number of leads present). Findings in ≥ Moderate Risk and Low Risk groups were compared.

Results: The cohort comprises 18 patients (78% probands, 72% male, mean age 39 ± 14 years). There were 7 (39%) patients classified as ≥ Moderate Risk and 11 (61%) as Low Risk. Prior spontaneous type 1 ECG was present in 6 (33%). Two patients had prior aborted cardiac arrest. An intermittent type 1 ECG was seen for ≥1 hour in 5 (28%) patients.

≥ Moderate Risk patients displayed a higher ‘type 1 burden’ in standard and high RV leads (18.0 ± 26.7 versus 0.1 ± 0.3 lead.hours, p=0.04) and sum J-point elevation over 24 hours (22.3 ± 27.6 versus 2.3 ± 3.3 mV, p=0.03) than low risk patients (see Figure 1). Prospective data collection and analysis is ongoing.

Conclusions: Ambulatory 12-lead ECG differentiates low risk from
≥ Moderate Risk patients and may be superior to ajmaline provocation in identifying patients with prognostically significant BrS. Sum J-point elevation over 24 hours may represent a novel risk marker for arrhythmic events in BrS.

 

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