Body Surface Mapping system - a potential diagnostic tool for unmasking delayed right ventricular epicardial activation in ARVC patients and phenotype-negative gene-carriers

• Published in: Europace (London, England) England), 2022-05, Vol.24 (Supplement_1)
• Main Authors: Kommata, B, Sciaraffia, E, Blomstrom- Lundqvist, C
• Format: Article
• Language: English
• ISSN: 1099-5129; 1532-2092
• DOI: 10.1093/europace/euac053.035

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Selanders stiftelsen Background Life-threatening ventricular arrhythmias can occur at any stages of ARVC – the detection of early manifestations of the disease may have prognostic implications. Purpose The purpose was to explore the usefulness of a 252-leads noninvasive Body Surface Mapping (BSM) system for the detection of delayed epicardial activation in ARVC patients and phenotype-negative gene-carriers (GC). Methods Twelve patients with ARVC, 20 GC and 8 genotype and phenotype negative family members served as controls (C) were included. 12-lead ECG, signal-averaged-electrocardiogram, echocardiography, 252-lead BSM recordings and thoracic CT scan were performed in all subjects. The noninvasively reconstructed epicardial signals of the right ventricle (RV) were analysed using the Activation Time Editing tool of the BSM system. Local depolarisation was defined as the steepest negative dV/dt of the local epicardial signal. The time from the start of RV epicardial signals to the earliest local depolarisation (ELD) and to the latest local depolarisation (LLD), were measured for the whole RV and separately for the anterior free wall (AW) and inferior wall (IW). The duration of the activation, defined as LLD-ELD, was calculated for AW, IW and the whole RV. Results The ELDs was similar in all study groups whereas the LLD in the IW and whole RV was significantly longer among ARVC patients compared to C. Although the activation durations in the AW and IW did not differ between the groups, the activation duration of the whole RV was significantly longer in ARVC patients. A LLD cut off of 81ms in RV and an activation duration cut off of 49msec in RV discriminated ARVC patients from C with highest sensitivity and specificity. Based on these cut-offs, 35% of GC group had longer LLD times and 70 % had longer activation duration (figure 1). Conclusions ARVC patients as well as the majority of GC demonstrated prolonged LLD and/or activation duration times in RV compared to C, suggesting that the 252-leads noninvasive BSM system may be a useful tool for early detection of delayed RV epicardial activations. Larger studies are required to confirm our results. Figure 1