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Hypertension is the leading modifiable risk factor for global cardiovascular disease, responsible for an estimated 10.8 million deaths and more than 200 million disability-adjusted life years annually.1 Despite the availability of effective pharmacological and lifestyle interventions, prevalence continues to rise, particularly in low- and middle-income countries (LMICs), where over three-quarters of all cases now occur.2 The condition’s […]

198/The response to sodium channel provocation in healthy subjects

BE Ensam (Presenting Author) – St Georges University of London, London, UK; SC Scrocco – St Georges University of London, London, UK; VB Batchvarov – St Georges University of London, London, UK; GF Finocchario – St Georges University of London, London, UK; SC Papatheodorou – St Georges University of London, London, UK; C Miles – St Georges University of London, London, UK; B Gray – St Georges University of London, London, UK; E Behr – St Georges University of London, London, UK
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Published Online: Oct 4th 2008 European Journal of Arrhythmia & Electrophysiology. 2019;5(Suppl. 1):abstr198
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Article

Abstract: Sodium channel blockade (SCB) is used to investigate those thought to be at risk of harbouring a concealed form of Brugada syndrome (BRS). Most frequently this includes those undergoing evaluation following cardiac arrest, or a premature sudden death or diagnosis of BRS in a relative. However, a recent consensus document advised that an isolated drug induced type 1 Brugada ECG pattern is no longer diagnostic of BRS. This followed identification of an ajmaline induced type 1 pattern in 4.5% of undefined controls in a small Turkish study. The primary objective of this study was not, however, the yield of SCB in health subjects. Thus, the precise yield of the type 1 pattern in systematically evaluated healthy subjects remains unknown.

Objective: To determine the yield of the drug induced type 1 pattern in systematically evaluated healthy subjects undergoing SCB with Ajmaline.

Methods: Potential volunteers responded to a national advertisement for healthy subjects. Following a comprehensive online screening questionnaire regarding personal and family history, eligible participants were invited to undergo pre-trial screening which involved a focussed cardiovascular history and examination, high-right-precordial-lead electrocardiography (HRPL-ECG) and transthoracic echocardiography (ECHO). Those with a pre-screening abnormality were excluded. Finally, eligible subjects underwent intravenous Ajmaline provocation using a standard protocol (1 mg/kg max 100 mg over 5 minutes) with continuous digital HRPL-ECG acquisition followed by a 24-hour ambulatory HRPL-ECG and a contrast enhanced cardiac magnetic resonance scan (CMR).

Results: From 340 online responses, 204 were deemed eligible based on the screening questionnaire and were invited for pre-trial screening. One-hundred-and-ten (110) subjects attended, of whom 100 were deemed eligible and underwent Ajmaline provocation. Three subjects (3/100 3%) developed the diagnostic type 1 BRS pattern (see Figure 1). A spontaneous type 1 pattern was not observed in any subject during ambulatory HRPL-ECG monitoring.

Conclusion: The yield of the ajmaline-induced type 1 Brugada ECG pattern in comprehensively screened healthy subjects is 3% (3/100). Robust revision of the diagnostic criteria for ajmaline challenge in BRS are necessary.

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