Abstract
Background: 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.Methods and Results: 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 Ca2+ 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 Ca2+ 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).Conclusion: 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.
Highlights
Interruption of myocardial blood flow due to narrowing or blocking of coronary arteries leads to cell damage and death in the areas of tissue supplied by these vessels
Sparse regions of residual myocardium survive through the healing process and can be detected in the scar embedded in fibrous tissue, both histologically (Camelliti et al, 2004; Walker et al, 2007) and using live tissue imaging techniques, including optical coherence tomography and twophoton microscopy (Goergen et al, 2016)
In the case of the normal zone (NZ) and the border to the NZ (BZ), the relative uniformity of the action potential (AP) signal recorded with the 10× objective allowed 40× imaging to be made routinely in the center of the field of view
Summary
Interruption of myocardial blood flow due to narrowing or blocking of coronary arteries leads to cell damage and death in the areas of tissue supplied by these vessels. Following this myocardial infarction (MI), ischemia of the underlying muscle causes necrosis of cardiomyocytes and vasculature. Sparse regions of residual myocardium survive through the healing process and can be detected in the scar embedded in fibrous tissue, both histologically (Camelliti et al, 2004; Walker et al, 2007) and using live tissue imaging techniques, including optical coherence tomography and twophoton microscopy (Goergen et al, 2016). This study aims to examine the extent and nature of the residual electrical activity within a stabilized ventricular infarct scar
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