Human ventricular activation sequence and the simulation of the electrocardiographic QRS complex and its variability in healthy and intraventricular block conditions.
Human ventricular activation sequence and the simulation of the electrocardiographic QRS complex and its variability in healthy and intraventricular block conditions.
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DOI：
10.1093/europace/euw346
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发表时间：
2016-12
期刊：
影响因子：
--
通讯作者：
Rodriguez B
中科院分区：
文献类型：
--
作者：
Cardone-Noott L;Bueno-Orovio A;Mincholé A;Zemzemi N;Rodriguez B
研究激活序列和被动传导特性的变异性如何转化为QRS生物标志物的临床变异性，并获得关于人体QRS波群所含信息的新生理学知识。使用详细的心脏躯干人体解剖模型进行多尺度bidomain模拟，以研究激活序列特征对临床QRS生物标志物的影响。构建激活序列并针对实验衍生的离体和体内人激活数据进行验证。R峰振幅在QRS形态方面表现出最大的变异性，这是由于其同时受到激活序列速度、心肌细胞内和细胞外电导率以及通过人体躯干传播的调制。然而，QRS宽度受内皮细胞激活速度和细胞内心肌电导率的调节，而QR间期仅受内皮细胞激活曲线的影响。左室前壁和后壁激动部位的心尖-基底位置的变异性分别与肢体和心前区导联的S波进展以及心前区导联偶见的切迹QRS波群相关。早期激活位点数量的变异性成功地再现了QRS波群中人类传导系统的病理异常。激活序列和被动传导特性的变异性捕获并解释了在人体QRS波群中观察到的大部分临床变异性。我们的生理学见解允许在QRS形态和早期内皮素激活位点的位置方面对人类QRS生物标志物进行更深入的解释。这可能是用来获得一个更好的病人特定的知识激活序列从常规体表心电图。
To investigate how variability in activation sequence and passive conduction properties translates into clinical variability in QRS biomarkers, and gain novel physiological knowledge on the information contained in the human QRS complex. Multiscale bidomain simulations using a detailed heart-torso human anatomical model are performed to investigate the impact of activation sequence characteristics on clinical QRS biomarkers. Activation sequences are built and validated against experimentally-derived ex vivo and in vivo human activation data. R-peak amplitude exhibits the largest variability in terms of QRS morphology, due to its simultaneous modulation by activation sequence speed, myocardial intracellular and extracellular conductivities, and propagation through the human torso. QRS width, however, is regulated by endocardial activation speed and intracellular myocardial conductivities, whereas QR intervals are only affected by the endocardial activation profile. Variability in the apico-basal location of activation sites on the anterior and posterior left ventricular wall is associated with S-wave progression in limb and precordial leads, respectively, and occasional notched QRS complexes in precordial derivations. Variability in the number of early activation sites successfully reproduces pathological abnormalities of the human conduction system in the QRS complex. Variability in activation sequence and passive conduction properties captures and explains a large part of the clinical variability observed in the human QRS complex. Our physiological insights allow for a deeper interpretation of human QRS biomarkers in terms of QRS morphology and location of early endocardial activation sites. This might be used to attain a better patient-specific knowledge of activation sequence from routine body-surface electrocardiograms.