University of Sydney, Sydney, Australia.
Department of Cardiology, Westmead Hospital, Sydney, Australia.
PLoS One. 2018 Oct 5;13(10):e0204997. doi: 10.1371/journal.pone.0204997. eCollection 2018.
Post-myocardial infarction (MI) remodeling contributes to increased electrophysiological and structural heterogeneity and arrhythmogenesis. Utilising the post-infarct ovine model our aim was to determine unipolar electrogram frequency characteristics consequent to this remodeling and the development of Ventricular Tachycardia (VT).
Mapping studies were performed on 14 sheep at >1 month post-MI induction. Sheep were divided into VT inducible (n = 7) and non-inducible (n = 7) groups. Multielectrode needles (n = 20) were deployed within and surrounding ventricular scar for electrophysiological assessment of electrogram amplitude and width. Spectral analysis of electrograms was undertaken using wavelet and fast fourier transformations (WFFT) to calculate root mean square (RMS) power intervals spanning 0-300Hz in 20Hz intervals. Quantitative assessment between electrophysiological and histological parameters including collagen density, and structural organization of the myocardium was performed. Increasing myocardial scar density resulted in attenuation of electrogram amplitude and RMS values. (all p<0.01). Between groups there were no differences in electrogram amplitude (p = 0.37), however WFFT analysis revealed significantly higher RMS values in the VT group (p<0.05) in association with high frequency fractional components of the electrogram. As scar density increased, greater between-group differences in RMS were observed spanning this high frequency (200-280Hz) spectrum and which were proportionally dependent on the degree of structural disorganisation of the myocardium (p<0.001) and number of extrastimuli required to induce VT (p<0.05).
High frequency unipolar electrogram spectral characteristics were quantitatively co-influenced by the presence of fibrosis and degree of myocardial structural dissorganisation and were associated with the propensity for development of VT.
心肌梗死后(MI)重构导致电生理和结构异质性增加,从而引发心律失常。本研究利用梗死后的绵羊模型,旨在确定这种重构后单相心内膜电图(unipolar electrogram)频率特征与室性心动过速(VT)的发生。
在 MI 诱导后>1 个月,对 14 只绵羊进行了映射研究。绵羊分为 VT 可诱导组(n = 7)和非诱导组(n = 7)。在心室瘢痕内和周围部署多电极针(n = 20),以评估心内膜电图振幅和宽度的电生理特性。使用小波和快速傅里叶变换(WFFT)对心内膜电图进行频谱分析,以计算跨越 0-300Hz 的均方根(RMS)功率间隔,间隔为 20Hz。对电生理和组织学参数(包括胶原密度和心肌结构组织)进行定量评估。随着心肌瘢痕密度的增加,心内膜电图振幅和 RMS 值逐渐降低(均 P<0.01)。两组间心内膜电图振幅无差异(P = 0.37),但 VT 组的 WFFT 分析显示 RMS 值显著升高(P<0.05),与心内膜电图的高频分数成分相关。随着瘢痕密度的增加,在这个高频(200-280Hz)频谱中,两组间 RMS 的差异逐渐增大,这与心肌结构紊乱的程度呈比例相关(P<0.001),并且与诱发 VT 所需的额外刺激数也呈比例相关(P<0.05)。
高频单相心内膜电图频谱特征受纤维化和心肌结构紊乱程度的共同影响,并与 VT 的发生倾向相关。