Abstract

BackgroundVentricular fibrillation (VF) is the main cause of sudden cardiac death, but its mechanisms are still unclear. We propose a noninvasive approach to describe the progression of VF complexity from body surface potential maps (BSPMs).MethodsWe mapped 252 VF episodes (16 ± 10 s) with a 252-electrode vest in 110 patients (89 male, 47 ± 18 years): 50 terminated spontaneously, otherwise by electrical cardioversion (DCC). Changes in complexity were assessed between the onset (“VF start”) and the end (“VF end”) of VF by the nondipolar component index (NDIBSPM), measuring the fraction of energy nonpreserved by an equivalent 3D dipole from BSPMs. Higher NDI reflected lower VF organization. We also examined other standard body surface markers of VF dynamics, including fibrillatory wave amplitude (ABSPM), surface cycle length (BsCLBSPM) and Shannon entropy (ShEnBSPM). Differences between patients with and without structural heart diseases (SHD, 32 vs. NSHD, 78) were also tested at those stages. Electrocardiographic features were validated with simultaneous endocardium cycle length (CL) in a subset of 30 patients.ResultsAll BSPM markers measure an increase in electrical complexity during VF (p < 0.0001), and more significantly in NSHD patients. Complexity is significantly higher at the end of sustained VF episodes requiring DCC. Intraepisode intracardiac CL shortening (VF start 197 ± 24 vs. VF end 169 ± 20 ms; p < 0.0001) correlates with an increase in NDI, and decline in surface CL, f-wave amplitude, and entropy (p < 0.0001). In SHD patients VF is initially more complex than in NSHD patients (NDIBSPM, p = 0.0007; ShEnBSPM, p < 0.0001), with moderately slower (BsCLBSPM, p = 0.06), low-amplitude f-waves (ABSPM, p < 0.0001). In this population, lower NDI (p = 0.004) and slower surface CL (p = 0.008) at early stage of VF predict self-termination. In the NSHD group, a more abrupt increase in VF complexity is quantified by all BSPM parameters during sustained VF (p < 0.0001), whereas arrhythmia evolution is stable during self-terminating episodes, hinting at additional mechanisms driving VF dynamics.ConclusionMultilead BSPM analysis underlines distinct degrees of VF complexity based on substrate characteristics.

Highlights

  • Sudden cardiac death is a major health problem worldwide accounting for 8% to 12% of all deaths (Hayashi et al, 2015), with global annual incidence rates between 50 and 100 per 100,000 cases (Fishman et al, 2010).Ventricular fibrillation is the most serious heart rhythm disturbance and the main cause of sudden cardiac death (SCD) (Priori et al, 2015)

  • All body surface potential mapping (BSPM) markers measure an increase in electrical complexity during Ventricular fibrillation (VF) (p < 0.0001), and more significantly in no structural heart disease(s) (NSHD) patients

  • In the NSHD group, a more abrupt increase in VF complexity is quantified by all BSPM parameters during sustained VF (p < 0.0001), whereas arrhythmia

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Summary

Introduction

Sudden cardiac death is a major health problem worldwide accounting for 8% to 12% of all deaths (Hayashi et al, 2015), with global annual incidence rates between 50 and 100 per 100,000 cases (Fishman et al, 2010).Ventricular fibrillation is the most serious heart rhythm disturbance and the main cause of SCD (Priori et al, 2015). The development of multielectrode (Rogers et al, 1999) and optical mapping (Park and Gray, 2015) techniques for the analysis of the electrical activation of the myocardium has enabled a more detailed evaluation of the electrical substrate of the arrhythmia, and both multiple wavelet and mother rotor hypotheses have been thought to be involved in VF initiation and maintenance (Jalife, 2000; Weiss et al, 2005). Despite such advances, the mechanisms underlying this electrical disorder are still controversial. We propose a noninvasive approach to describe the progression of VF complexity from body surface potential maps (BSPMs)

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