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致心律失常药物可放大豚鼠离体心脏电恢复过程中的空间异质性:来自单相动作电位时程和JT间期评估的证据。

Arrhythmogenic drugs can amplify spatial heterogeneities in the electrical restitution in perfused guinea-pig heart: An evidence from assessments of monophasic action potential durations and JT intervals.

作者信息

Osadchii Oleg E

机构信息

Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.

Department of Health Science and Technology, University of Aalborg, Aalborg, Denmark.

出版信息

PLoS One. 2018 Jan 19;13(1):e0191514. doi: 10.1371/journal.pone.0191514. eCollection 2018.

Abstract

Non-uniform shortening of the action potential duration (APD90) in different myocardial regions upon heart rate acceleration can set abnormal repolarization gradients and promote arrhythmia. This study examined whether spatial heterogeneities in APD90 restitution can be amplified by drugs with clinically proved proarrhythmic potential (dofetilide, quinidine, procainamide, and flecainide) and, if so, whether these effects can translate to the appropriate changes of the ECG metrics of ventricular repolarization, such as JT intervals. In isolated, perfused guinea-pig heart preparations, monophasic action potentials and volume-conducted ECG were recorded at progressively increased pacing rates. The APD90 measured at distinct ventricular sites, as well as the JTpeak and JTend values were plotted as a function of preceding diastolic interval, and the maximum slopes of the restitution curves were determined at baseline and upon drug administration. Dofetilide, quinidine, and procainamide reverse rate-dependently prolonged APD90 and steepened the restitution curve, with effects being greater at the endocardium than epicardium, and in the right ventricular (RV) vs. the left ventricular (LV) chamber. The restitution slope was increased to a greater extent for the JTend vs. the JTpeak interval. In contrast, flecainide reduced the APD90 restitution slope at LV epicardium without producing effect at LV endocardium and RV epicardium, and reduced the JTpeak restitution slope without changing the JTend restitution. Nevertheless, with all agents, these effects translated to the amplified epicardial-to-endocardial and the LV-to-RV non-uniformities in APD90 restitution, paralleled by the increased JTend vs. JTpeak difference in the restitution slope. In summary, these findings suggest that arrhythmic drug profiles are partly attributable to the accentuated regional heterogeneities in APD90 restitution, which can be indirectly determined through ECG assessments of the JTend vs. JTpeak dynamics at variable pacing rates.

摘要

心率加快时不同心肌区域动作电位时程(APD90)的不均一缩短可设置异常复极梯度并促进心律失常。本研究检测了具有临床证实的致心律失常潜能的药物(多非利特、奎尼丁、普鲁卡因胺和氟卡尼)是否能放大APD90恢复的空间异质性,如果是,这些效应是否能转化为心室复极心电图指标(如JT间期)的适当变化。在离体灌注豚鼠心脏标本中,在逐渐增加的起搏频率下记录单相动作电位和容积传导心电图。将在不同心室部位测得的APD90以及JTpeak和JTend值绘制为前一心舒张间期的函数,并在基线和给药后确定恢复曲线的最大斜率。多非利特、奎尼丁和普鲁卡因胺呈心率依赖性地延长APD90并使恢复曲线变陡,在心内膜的效应大于心外膜,在右心室(RV)比左心室(LV)腔更明显。JTend间期的恢复斜率比JTpeak间期增加得更多。相比之下,氟卡尼降低了左心室心外膜的APD90恢复斜率,而对左心室心内膜和右心室心外膜无影响,降低了JTpeak恢复斜率而不改变JTend恢复斜率。然而,使用所有药物时,这些效应都转化为APD90恢复中心外膜到心内膜以及左心室到右心室的不均一性放大,同时JTend与JTpeak恢复斜率差异增加。总之,这些发现表明,心律失常药物的特征部分归因于APD90恢复中区域异质性的加剧,这可以通过在可变起搏频率下对JTend与JTpeak动态进行心电图评估间接确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a20/5774816/d06f1b798187/pone.0191514.g001.jpg

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