Key result
Body surface mapping QRS dispersion distinguishes ARVC from controls using a 40 ms cut-off.
Why the study?
The diagnosis of ARVC remains complex, motivating investigation into whether QRS dispersion assessed by body surface mapping could detect early signs of ARVC, particularly in gene carriers.
Does QRS dispersion assessed by 252-lead body surface mapping improve the detection of early signs of ARVC compared to 12-lead ECG in ARVC patients and healthy gene carriers?
Cross-Sectional (n=40)
Does QRS dispersion assessed by 252-lead body surface mapping improve the detection of early signs of ARVC compared to 12-lead ECG in ARVC patients and healthy gene carriers?
QRS dispersion assessed by 252-lead body surface mapping better distinguishes ARVC patients from controls compared to 12-lead ECG and may detect early depolarization changes in healthy gene carriers.
May signal early ARVC changes in gene carriers; hypothesis-generating and should not yet change practice.
BACKGROUND: The diagnosis of ARVC remains complex requiring both imaging and electrocardiographic (ECG) techniques. The purpose was therefore to investigate whether QRS dispersion assessed by body surface mapping (BSM) could be used to detect early signs of ARVC, particularly in gene carriers. METHODS: ARVC patients, gene carriers without a history of arrhythmias or structural cardiac changes and healthy controls underwent 12-lead resting ECG, signal-averaged ECG, echocardiographic examination, 24-hours Holter monitoring, and BSM with electrocardiographic imaging. All 252-leads BSM recordings and 12-leads ECG recordings were manually analyzed for QRS durations and QRS dispersion. RESULTS: Eight controls, 12 ARVC patients with definite ARVC and 20 healthy gene carriers were included. The ECG-QRS dispersion was significantly greater in ARVC patients (42 vs. 25 ms, p < .05), but failed to fully differentiate them from controls. The BSM-derived QRS dispersion was also significantly greater in ARVC patients versus controls (65 vs. 29 ms, p < .05) and distinguished 11/12 cases from controls using the cut-off 40msec. The BSM derived QRS dispersion was abnormal (> 40 ms) in 4/20 healthy gene carriers without signs of ARVC, which may indicate early depolarization changes. CONCLUSIONS: QRS dispersion, when assessed by BSM versus 12-lead ECG, seem to better distinguish ARVC patients from controls, and could potentially be used to detect early ARVC in gene carriers. Further studies are required to confirm the value of BSM-QRS dispersion in this respect.
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Kommata et al. (2021) conducted a cross-sectional in Arrhythmogenic right ventricular cardiomyopathy (ARVC) (n=40). Body surface mapping (BSM) derived QRS dispersion vs. 12-lead ECG QRS dispersion was evaluated on QRS dispersion (p=< .05). Body surface mapping-derived QRS dispersion was significantly greater in ARVC patients versus controls (65 vs. 29 ms, p < 0.05) and distinguished 11 of 12 cases using a 40 ms cut-off.
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