Three-dimensional myocardial scarring along myofibers after coronary ischemia-reperfusion revealed by computerized images of histological assays.
Three-dimensional myocardial scarring along myofibers after coronary ischemia-reperfusion revealed by computerized images of histological assays.
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DOI：
10.14814/phy2.12072
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发表时间：
2014-07-16
影响因子：
2.5
通讯作者：
Matsui T
中科院分区：
文献类型：
--
作者：
Katz MY;Kusakari Y;Aoyagi H;Higa JK;Xiao CY;Abdelkarim AZ;Marh K;Aoyagi T;Rosenzweig A;Lozanoff S;Matsui T
急性心肌梗死后左心室（LV）不良重构的特征是LV扩张和纤维化瘢痕的发展，并且是心力衰竭后续发展的预后的关键因素。虽然肌纤维组织被认为是重要的保存生理心脏功能和结构，损伤的肌纤维在左心室重塑的解剖特征尚未完全确定。在冠状动脉左前降支结扎诱导的缺血再灌注（I/R）损伤的小鼠模型中，我们先前的组织学分析表明，广泛的纤维化瘢痕从最初的梗死区延伸到远端区，并沿沿着中周肌纤维清楚地划分。此外，在内膜下和心外膜下的纵向肌纤维中未观察到纤维化。然而，组织切片的组织学分析不能充分表明整个心脏的肌纤维损伤分布。为了解决这个问题，我们使用从I/R损伤小鼠心脏的多个组织切片获得的三维（3D）图像研究了沿着肌纤维的瘢痕形成模式。在3D图像中观察到的纤维化瘢痕区域与中周肌纤维的分布一致。在顶端，瘢痕形成沿着肌纤维沿着形成一个不完整的C形环，该环向末端会聚成三角形。我们的研究结果表明，短暂冠状动脉结扎后的心肌细胞损伤沿着肌纤维延伸，而不是沿着冠状动脉穿透心肌的路径。心肌缺血再灌注损伤后沿着肌纤维观察到的损伤模式可用于预测心肌梗死患者的预后。在冠状动脉左前降支结扎诱导的缺血-再灌注损伤小鼠模型中，从组织切片（实心黄色区域）获得的心肌瘢痕的三维图像表明，瘢痕从基部依次延伸到中部的顶点。在顶点处，瘢痕形成沿着肌纤维沿着形成不完整的C形环，该C形环朝向末端会聚成三角形。这些发现表明，短暂冠状动脉结扎后的心肌细胞损伤沿着肌纤维延伸，而不是沿着冠状动脉穿透心肌的路径。
Adverse left ventricular (LV) remodeling after acute myocardial infarction is characterized by LV dilatation and development of a fibrotic scar, and is a critical factor for the prognosis of subsequent development of heart failure. Although myofiber organization is recognized as being important for preserving physiological cardiac function and structure, the anatomical features of injured myofibers during LV remodeling have not been fully defined. In a mouse model of ischemia–reperfusion (I/R) injury induced by left anterior descending coronary artery ligation, our previous histological assays demonstrated that broad fibrotic scarring extended from the initial infarct zone to the remote zone, and was clearly demarcated along midcircumferential myofibers. Additionally, no fibrosis was observed in longitudinal myofibers in the subendocardium and subepicardium. However, a histological analysis of tissue sections does not adequately indicate myofiber injury distribution throughout the entire heart. To address this, we investigated patterns of scar formation along myofibers using three‐dimensional (3D) images obtained from multiple tissue sections from mouse hearts subjected to I/R injury. The fibrotic scar area observed in the 3D images was consistent with the distribution of the midcircumferential myofibers. At the apex, the scar formation tracked along the myofibers in an incomplete C‐shaped ring that converged to a triangular shape toward the end. Our findings suggest that myocyte injury after transient coronary ligation extends along myofibers, rather than following the path of coronary arteries penetrating the myocardium. The injury pattern observed along myofibers after I/R injury could be used to predict prognoses for patients with myocardial infarction. In a mouse model of ischemia–reperfusion injury induced by left anterior descending coronary artery ligation, three‐dimensional images of myocardial scarring obtained from tissue sections (solid yellow area) indicate that the scar sequentially extends from the base to the apex in the midcardium. At the apex, the scar formation tracks along the myofibers in an incomplete C‐shaped ring that converges to a triangular shape toward the end. These findings suggest that myocyte injury after transient coronary ligation extends along myofibers, rather than following the path of coronary arteries penetrating the myocardium.