Department of Forensic Medicine, Hebei Medical University, No, 361 Zhongshan Road, Shijiazhuang, Hebei 050017, China.
Diagn Pathol. 2013 May 17;8:84. doi: 10.1186/1746-1596-8-84.
Sudden cardiac death resulting from acute myocardial infarction (AMI) constitutes a significant percentage of the caseload for forensic and clinical pathologists. When sudden death occurs at an early stage (<6 h), pathologists experience difficulty in the postmortem diagnosis of AMI. Because of the specific tissue distribution of S100A1 and its relationship with acute ischemic heart disease, this study aimed to evaluate the performance of S100A1 in the postmortem diagnosis of AMI.
We constructed a rat model of AMI through permanent ligation of the left anterior descending coronary artery (LAD) to investigate the depletion of S100A1 from ischemic cardiomyocytes by immunohistochemistry and measuring S100A1 plasma concentrations by enzyme-linked immunosorbent assay at varying post-infarction intervals. In addition, immunohistochemical staining of S100A1 for definite infarction, suspected early infarction, and in normal human hearts, was also performed to test its practical feasibility for postmortem diagnosis of AMI at an early stage.
As early as 15 min after ligation of the LAD, depletion of S100A1 was observed in ischemic cardiomyocytes, and S100A1 plasma concentration was also significantly higher than that of the sham-operated group (P < 0.001). With continuation of the occlusion time, the depleted areas of S100A1 further expanded and S100A1 plasma concentrations further increased. For autopsy material, all human cases of definite myocardial infarction and suspected early infarction showed well-defined areas without S100A1 staining. None of the normal human cases showed diffuse depletion of S100A1.
Our results suggest that immunohistochemical detection of S100A1 is useful for the postmortem diagnosis of AMI at an early stage.
The virtual slide(s) for this article can be found here:http://www.diagnosticpathology.diagnomx.eu/vs/4366650979519818.
急性心肌梗死(AMI)导致的心脏性猝死在法医和临床病理学家的病例中占很大比例。当早期(<6 小时)发生猝死时,病理学家在 AMI 的死后诊断中遇到困难。由于 S100A1 的特定组织分布及其与急性缺血性心脏病的关系,本研究旨在评估 S100A1 在 AMI 死后诊断中的性能。
通过永久性结扎左前降支冠状动脉(LAD)构建 AMI 大鼠模型,通过免疫组织化学检测缺血性心肌细胞中 S100A1 的耗竭,并通过酶联免疫吸附试验测量不同梗死间隔后 S100A1 的血浆浓度。此外,还对 S100A1 在明确梗死、疑似早期梗死和正常人心肌中的免疫组织化学染色进行了检测,以测试其在早期进行 AMI 死后诊断的实际可行性。
结扎 LAD 后 15 分钟即可观察到缺血性心肌细胞中 S100A1 的耗竭,S100A1 血浆浓度也明显高于假手术组(P<0.001)。随着闭塞时间的延长,S100A1 耗竭的区域进一步扩大,S100A1 血浆浓度进一步升高。对于尸检材料,所有明确的心肌梗死和疑似早期梗死的人类病例均显示无 S100A1 染色的明确区域。没有一例正常人类病例显示 S100A1 弥漫性耗竭。
我们的结果表明,免疫组织化学检测 S100A1 对早期 AMI 的死后诊断有用。