Ghouri Iffath A, Kelly Allen, Salerno Simona, Garten Karin, Stølen Tomas, Kemi Ole-Johan, Smith Godfrey L
Institute of Cardiovascular & Medical Sciences, University of Glasgow, Glasgow, United Kingdom.
Department of Circulation and Medical Imaging, St. Olav's Hospital, Norwegian University of Science and Technology, Trondheim, Norway.
Front Physiol. 2018 Oct 17;9:1454. doi: 10.3389/fphys.2018.01454. eCollection 2018.
The origin of electrical behavior in post-myocardial infarction scar tissue is still under debate. This study aims to examine the extent and nature of the residual electrical activity within a stabilized ventricular infarct scar. An apical infarct was induced in the left ventricle of Wistar rats by coronary artery occlusion. Five weeks post-procedure, hearts were Langendorff-perfused, and optically mapped using di-4-ANEPPS. Widefield imaging of optical action potentials (APs) on the left ventricular epicardial surface revealed uniform areas of electrical activity in both normal zone (NZ) and infarct border zone (BZ), but only limited areas of low-amplitude signals in the infarct zone (IZ). 2-photon (2P) excitation of di-4-ANEPPS and Fura-2/AM at discrete layers in the NZ revealed APs and Ca transients (CaTs) to 500-600 μm below the epicardial surface. 2P imaging in the BZ revealed superficial connective tissue structures lacking APs or CaTs. At depths greater than approximately 300 μm, myocardial structures were evident that supported normal APs and CaTs. In the IZ, although 2P imaging did not reveal clear myocardial structures, low-amplitude AP signals were recorded at discrete layers. No discernible Ca signals could be detected in the IZ. AP rise times in BZ were slower than NZ (3.50 ± 0.50 ms vs. 2.23 ± 0.28 ms) and further slowed in IZ (9.13 ± 0.56 ms). Widefield measurements of activation delay between NZ and BZ showed negligible difference (3.37 ± 1.55 ms), while delay values in IZ showed large variation (11.88 ± 9.43 ms). These AP measurements indicate that BZ consists of an electrically inert scar above relatively normal myocardium. Discrete areas/layers of IZ displayed entrained APs with altered electrophysiology, but the structure of this tissue remains to be elucidated.
心肌梗死后瘢痕组织电活动的起源仍存在争议。本研究旨在探究稳定的心室梗死瘢痕内残余电活动的程度和性质。通过冠状动脉闭塞在Wistar大鼠左心室诱导心尖梗死。术后五周，对心脏进行Langendorff灌注，并使用di-4-ANEPPS进行光学标测。左心室心外膜表面光学动作电位（APs）的宽场成像显示，正常区（NZ）和梗死边缘区（BZ）均有均匀的电活动区域，但梗死区（IZ）仅有有限的低振幅信号区域。在NZ的离散层对di-4-ANEPPS和Fura-2/AM进行双光子（2P）激发，发现心外膜表面以下500 - 600μm处有APs和钙瞬变（CaTs）。BZ的2P成像显示浅表结缔组织结构缺乏APs或CaTs。在深度大于约300μm处，可见支持正常APs和CaTs的心肌结构。在IZ中，尽管2P成像未显示清晰的心肌结构，但在离散层记录到了低振幅AP信号。在IZ中未检测到可辨别的钙信号。BZ中AP的上升时间比NZ慢（3.50±0.50 ms对2.23±0.28 ms），在IZ中进一步减慢（9.13±0.56 ms）。NZ和BZ之间激活延迟的宽场测量显示差异可忽略不计（3.37±1.55 ms），而IZ中的延迟值变化较大（11.88±9.43 ms）。这些AP测量结果表明，BZ由相对正常心肌上方的电惰性瘢痕组成。IZ的离散区域/层显示出电生理改变的夹带APs，但该组织的结构仍有待阐明。
