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心室颤动动力学的心电图分析反映了缺血进展情况,该进展因患者解剖结构和电极位置的变异性而有所不同。

ECG analysis of ventricular fibrillation dynamics reflects ischaemic progression subject to variability in patient anatomy and electrode location.

作者信息

Martinez-Navarro Hector, Bertrand Ambre, Doste Ruben, Smith Hannah, Tomek Jakub, Ristagno Giuseppe, Oliveira Rafael S, Weber Dos Santos Rodrigo, Pandit Sandeep V, Rodriguez Blanca

机构信息

Department of Computer Science, British Heart Foundation Centre of Research Excellence, University of Oxford, Oxford, United Kingdom.

Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, United Kingdom.

出版信息

Front Cardiovasc Med. 2024 Nov 27;11:1408822. doi: 10.3389/fcvm.2024.1408822. eCollection 2024.

DOI:10.3389/fcvm.2024.1408822
PMID:39664764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11631900/
Abstract

BACKGROUND

Ventricular fibrillation (VF) is the deadliest arrhythmia, often caused by myocardial ischaemia. VF patients require urgent intervention planned quickly and non-invasively. However, the accuracy with which electrocardiographic (ECG) markers reflect the underlying arrhythmic substrate is unknown.

METHODS

We analysed how ECG metrics reflect the fibrillatory dynamics of electrical excitation and ischaemic substrate. For this, we developed a human-based computational modelling and simulation framework for the quantification of ECG metrics, namely, frequency, slope, and amplitude spectrum area (AMSA) during VF in acute ischaemia for several electrode configurations. Simulations reproduced experimental and clinical findings in 21 scenarios presenting variability in the location and transmural extent of regional ischaemia, and severity of ischaemia in the remote myocardium secondary to VF.

RESULTS

Regional acute myocardial ischaemia facilitated re-entries, potentially breaking up into VF. Ischaemia in the remote myocardium modulated fibrillation dynamics. Cases presenting a mildly ischaemic remote myocardium yielded sustained VF, enabled by the high proliferation of phase singularities (PS, 11-22) causing remarkably disorganised activation patterns. Conversely, global acute ischaemia induced stable rotors (3-12 PS). Changes in frequency and morphology of the ECG during VF reproduced clinical findings but did not show a direct correlation with the underlying wave dynamics. AMSA allowed the precise stratification of VF according to ischaemic severity in the remote myocardium (healthy: 23.62-24.45 mV Hz; mild ischaemia: 10.58-21.47 mV Hz; moderate ischaemia: 4.82-11.12 mV Hz). Within the context of clinical reference values, apex-anterior and apex-posterior electrode configurations were the most discriminatory in stratifying VF based on the underlying ischaemic substrate.

CONCLUSION

This study provides further insights into non-invasive patient-specific strategies for assessing acute ventricular arrhythmias. The use of reliable ECG markers to characterise VF is critical for developing tailored resuscitation strategies.

摘要

背景

心室颤动(VF)是最致命的心律失常,通常由心肌缺血引起。VF患者需要迅速且无创地制定紧急干预计划。然而,心电图(ECG)标志物反映潜在心律失常基质的准确性尚不清楚。

方法

我们分析了ECG指标如何反映电兴奋的颤动动力学和缺血基质。为此,我们开发了一个基于人体的计算建模和模拟框架,用于量化ECG指标,即急性缺血时VF期间几种电极配置下的频率、斜率和振幅谱面积(AMSA)。模拟重现了21种情况下的实验和临床结果,这些情况呈现出局部缺血的位置和透壁范围以及VF继发的远隔心肌缺血严重程度的变化。

结果

局部急性心肌缺血促进了折返,可能发展为VF。远隔心肌缺血调节颤动动力学。远隔心肌轻度缺血的病例产生持续性VF,这是由相位奇点(PS,11 - 22)的高度增殖导致明显紊乱的激活模式所促成的。相反,全身性急性缺血诱导稳定的转子(3 - 12个PS)。VF期间ECG频率和形态的变化重现了临床结果,但与潜在的波动动力学没有直接相关性。AMSA能够根据远隔心肌的缺血严重程度对VF进行精确分层(健康:23.62 - 24.45 mV Hz;轻度缺血:10.58 - 21.47 mV Hz;中度缺血:4.82 - 11.12 mV Hz)。在临床参考值范围内,心尖 - 前壁和心尖 - 后壁电极配置在基于潜在缺血基质对VF进行分层方面最具鉴别力。

结论

本研究为评估急性室性心律失常的无创个体化策略提供了进一步的见解。使用可靠的ECG标志物来表征VF对于制定个性化的复苏策略至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/88f74ef9e763/fcvm-11-1408822-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/ffa890eac1c7/fcvm-11-1408822-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/837051930725/fcvm-11-1408822-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/88f74ef9e763/fcvm-11-1408822-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/ffa890eac1c7/fcvm-11-1408822-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/3a009f2abc6b/fcvm-11-1408822-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/837051930725/fcvm-11-1408822-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/91ca64f20224/fcvm-11-1408822-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c747/11631900/88f74ef9e763/fcvm-11-1408822-g006.jpg

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