Determining anatomical and electrophysiological detail requirements for computational ventricular models of porcine myocardial infarction.

Determining anatomical and electrophysiological detail requirements for computational ventricular models of porcine myocardial infarction.
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DOI:
10.1016/j.compbiomed.2021.105061
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发表时间:
2022-03
影响因子:
7.7
通讯作者:
Bishop MJ
Bishop MJ
中科院分区:
工程技术2区
文献类型:
--
作者:
Mendonca Costa C;Gemmell P;Elliott MK;Whitaker J;Campos FO;Strocchi M;Neic A;Gillette K;Vigmond E;Plank G;Razavi R;O'Neill M;Rinaldi CA;Bishop MJ

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根据心脏MRI和电生理学(EP)数据建立的心脏计算模型已显示出预测心肌梗死(MI)相关室性心动过速(VT)风险和消融靶点以及预测心力衰竭患者起搏激动序列的前景。然而,最近的大多数研究依赖于低分辨率成像数据和很少或没有EP个性化,这可能会影响基于模型的预测的准确性。调查模型解剖结构、MI疤痕形态和EP个性化策略对起搏激动序列和VT诱导性的影响,以确定做出准确的基于模型的预测所需的细节水平。成像和EP数据采集自一组6只实验诱导MI的猪。构建了心室解剖结构的计算模型,包括MI瘢痕,包括双心室或仅左心室(LV)解剖结构和具有不同细节的MI瘢痕形态。除了相应的文献参数外,还分别使用QRS间期和QT间期将组织电导率和动作电位时程(APD)拟合至12导联ECG数据。模拟起搏激动序列和VT诱导。模拟起搏激动和VT诱导模型之间进行了比较,并对实验数据。模拟预测,模型解剖细节的水平对模拟起搏激活的影响很小,所有模型预测与侵入性EP测量密切相关。然而,需要高分辨率图像的详细疤痕形态、双心室解剖结构和个性化组织电导率来预测实验室性心动过速结局。本研究为基于临床数据的模型生成提供了明确的指导。虽然代表高水平的解剖和疤痕细节将需要高分辨率图像采集,但基于12导联ECG的EP个性化可以很容易地纳入建模流程,因为这些数据广泛可用。需要详细的瘢痕形态来模拟梗死相关心律失常。表示两个心室提高了心律失常模拟的准确性。模拟起搏激活不需要详细的解剖结构和疤痕形态。传导速度和组织电导率可以从ECG数据估计。基于ECG的参数提高了起搏和心律失常模拟的准确性。
Computational models of the heart built from cardiac MRI and electrophysiology (EP) data have shown promise for predicting the risk of and ablation targets for myocardial infarction (MI) related ventricular tachycardia (VT), as well as to predict paced activation sequences in heart failure patients. However, most recent studies have relied on low resolution imaging data and little or no EP personalisation, which may affect the accuracy of model-based predictions. To investigate the impact of model anatomy, MI scar morphology, and EP personalisation strategies on paced activation sequences and VT inducibility to determine the level of detail required to make accurate model-based predictions. Imaging and EP data were acquired from a cohort of six pigs with experimentally induced MI. Computational models of ventricular anatomy, incorporating MI scar, were constructed including bi-ventricular or left ventricular (LV) only anatomy, and MI scar morphology with varying detail. Tissue conductivities and action potential duration (APD) were fitted to 12-lead ECG data using the QRS duration and the QT interval, respectively, in addition to corresponding literature parameters. Paced activation sequences and VT induction were simulated. Simulated paced activation and VT inducibility were compared between models and against experimental data. Simulations predict that the level of model anatomical detail has little effect on simulated paced activation, with all model predictions comparing closely with invasive EP measurements. However, detailed scar morphology from high-resolution images, bi-ventricular anatomy, and personalized tissue conductivities are required to predict experimental VT outcome. This study provides clear guidance for model generation based on clinical data. While a representing high level of anatomical and scar detail will require high-resolution image acquisition, EP personalisation based on 12-lead ECG can be readily incorporated into modelling pipelines, as such data is widely available. Detailed scar morphology is required to simulate infarct-related arrhythmia. Representing both ventricles improves accuracy of arrhythmia simulations. Detailed anatomy and scar morphology are not required to simulate paced activation. Conduction velocities and tissue conductivities can be estimated from ECG data. ECG-based parameters improve accuracy of pacing and arrhythmia simulations.
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