ArticleHeart and vessels2017
Utility of 12-lead and signal-averaged Holter electrocardiograms after pilsicainide provocation for risk stratification in Brugada syndrome.
Article in Heart and vessels, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Effect of Mobile Internet on Attitude and Self-Efficacy of Patients with Coronary Heart Disease Diagnosed by 12-Lead Holter ECG.Journal of healthcare engineering · 2022Article
- Current Use and Future Needs of Noninvasive Ambulatory Electrocardiogram Monitoring.Internal medicine (Tokyo, Japan) · 2021Article
- Spectral Analysis of the QT Interval Increases the Prediction Accuracy of Clinical Variables in Brugada Syndrome.Journal of clinical medicine · 2019Article
- Prognostic Significance of the Sodium Channel Blocker Test in Patients With Brugada Syndrome.Journal of the American Heart Association · 2018Article
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6 authors.
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Abstract
Non-invasive risk stratification for ventricular fibrillation (VF) in Brugada syndrome (BrS) has not been fully evaluated. The aim of this study was to assess the utility of signal-averaged Holter electrocardiogram (Holter SAECG) and 12-lead Holter electrocardiogram (Holter ECG) after a pilsicainide provocation test for non-invasive risk stratification in BrS. We enrolled 30 consecutive patients with BrS [divided into 2 groups: the VF group, those with a previous history of VF (n = 10); and the non-VF group, those without a history of VF (n = 20)] and 10 control subjects without type 1 ECG. We evaluated late potentials [LP: filtered QRS (f-QRS), RMS40, and LAS40] on the Holter SAECG for 4 h after the pilsicainide provocation and in the same patients on another day without performing the pilsicainide provocation. Furthermore, we measured QRS duration and QTc interval in leads V2 and V5, and J amplitude in lead V2 on the Holter ECG after the pilsicainide provocation. On the Holter SAECG, the f-QRS at 1 h and LAS40 at 3 h after the pilsicainide provocation were significantly larger in the VF group than in the non-VF group (f-QRS at 1 h: 113.9 ± 8.9 vs. 104.9 ± 8 ms; p = 0.01, LAS40 at 3 h: 45.4 ± 5.9 vs. 35.5 ± 7.4 ms; p < 0.001). The receiver-operating characteristic curve analysis for a single parameter of VF occurrence was determined [f-QRS at 1 h: area under the curve (AUC) 0.8, with sensitivity 80% and specificity 80%; and LAS40 at 3 h: AUC 0.87, with sensitivity 90% and specificity 75%]. On the Holter ECG, there were no significant differences in these parameters between the VF and non-VF groups. In conclusion, the LP after the pilsicainide provocation using Holter SAECG may be useful for risk stratification of VF episodes in patients with BrS.
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