After myocardial infarction (MI), the infarcted tissue undergoes dynamic and time-dependent changes. Previous knowledge on MI biomechanical alterations has been obtained by studying the explanted scar tissues. In this study, we decellularized MI scar tissue and characterized the biomechanics of the obtained pure scar ECM. By thoroughly removing the cellular content in the MI scar tissue, we were able to avoid its confounding effects. Rat MI hearts were obtained from a reliable and reproducible model based on permanent left coronary artery ligation (PLCAL). MI heart explants at various time points (15 min, 1 week, 2 weeks, 4 weeks, and 12 weeks) were subjected to decellularization with 0.1% sodium dodecyl sulfate solution for ~1–2 weeks to obtain acellular scar ECM. A biaxial mechanical testing system was used to characterize the acellular scar ECM under physiologically relevant loading conditions. After decellularization, large decrease in wall thickness was observed in the native heart ECM and 15 min scar ECM, implying the collapse of cardiomyocyte lacunae after removal of heart muscle fibers. For scar ECM 1 week, 2 weeks, and 4 weeks post infarction, the decrease in wall thickness after decellularization was small. For scar ECM 12 weeks post infarction, the reduction amount of wall thickness due to decellularization was minimal. We found that the scar ECM preserved the overall mechanical anisotropy of the native ventricle wall and MI scar tissue, in which the longitudinal direction is more extensible. Acellular scar ECM from 15 min to 12 weeks post infarction showed an overall stiffening trend in biaxial behavior, in which longitudinal direction was mostly affected and manifested with a decreased extensibility and increased modulus. This reduction trend of longitudinal extensibility also led to a decreased anisotropy index in the scar ECM from the acute to chronic stages of MI. The post-MI change in biomechanical properties of the scar ECM reflected the alterations of collagen fiber network, confirmed by the histology of scar ECM. In short, the reported structure-property relationship reveals how scar ECM biophysical properties evolve from the acute to chronic stages of MI. The obtained information will help establish a knowledge basis about the dynamics of scar ECM to better understand post-MI cardiac remodeling.

心肌梗塞（MI）后，梗塞组织会经历动态且随时间变化的变化。先前关于 MI 生物力学改变的知识是通过研究外植的疤痕组织获得的。在这项研究中，我们对 MI 疤痕组织进行脱细胞处理，并表征了所获得的纯疤痕 ECM 的生物力学。通过彻底去除心肌梗死疤痕组织中的细胞内容物，我们能够避免其混淆效应。大鼠 MI 心脏是从基于永久左冠状动脉结扎 (PLCAL) 的可靠且可重复的模型中获得的。将不同时间点（15 分钟、1 周、2 周、4 周和 12 周）的 MI 心脏外植体用 0.1% 十二烷基硫酸钠溶液脱细胞约 1-2 周，以获得脱细胞疤痕 ECM。使用双轴机械测试系统来表征生理相关负载条件下的脱细胞疤痕 ECM。去细胞化后，在天然心脏ECM和15分钟疤痕ECM中观察到壁厚度大幅减少，这意味着去除心肌纤维后心肌细胞陷窝塌陷。对于梗塞后1周、2周和4周的疤痕ECM，脱细胞后壁厚度的减少很小。对于梗死后 12 周的疤痕 ECM，由于脱细胞化而导致的壁厚度减少量最小。我们发现，疤痕 ECM 保留了原生心室壁和 MI 疤痕组织的整体机械各向异性，其中纵向更具延展性。梗死后15分钟至12周的脱细胞疤痕ECM显示双轴行为总体僵化趋势，其中纵向受影响最大，表现为延展性下降和模量增加。 这种纵向延伸性的降低趋势也导致从急性心肌梗死到慢性心肌梗死阶段，疤痕ECM的各向异性指数降低。 MI 后疤痕 ECM 生物力学特性的变化反映了胶原纤维网络的变化，这已由疤痕 ECM 的组织学证实。简而言之，所报告的结构-性质关系揭示了疤痕 ECM 生物物理性质如何从 MI 的急性阶段演变为慢性阶段。获得的信息将有助于建立关于疤痕ECM动力学的知识基础，以更好地理解MI后心脏重塑。