Mair Johannes
Department of Internal Medicine III-Cardiology and Angiology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
J Clin Med. 2025 Jun 14;14(12):4241. doi: 10.3390/jcm14124241.
Current routine high-sensitivity cardiac troponin assays are the criterion standard for the laboratory diagnosis of myocardial injury due to their high analytical sensitivity and specificity. However, in daily clinical practice, unexpectedly elevated cardiac troponin test results without an obvious clinical correlate are becoming more frequent compared with previous cardiac troponin assay generations. In these patients, myocardial injury may sometimes be undetected by imaging techniques, including cardiac magnetic resonance imaging. This has led to an increased interest in the pathophysiology of cardiac troponin release, particularly with regard to whether troponin can be released in the absence of myocardial necrosis and thereby resulting in an increase in cardiac troponin in the systemic circulation. Although there is in vitro evidence that cardiac biomarkers are released from reversibly injured cultured cardiomyocytes, there is still a lack of evidence for cardiac troponin release apart from different forms of cell death (i.e., apoptosis or necrosis) in animal experiments. Conversely, various circulating cardiac troponin forms have been identified in human blood samples using different analytical methods, raising the question of whether the cause of myocardial injury can be reliably determined by measuring specific circulating cardiac troponin forms. Preliminary clinical data suggests that testing for specific circulating troponin forms could increase the specificity of cardiac troponin for diagnosing acute myocardial infarctions caused by an acute coronary syndrome. This review aims to provide an up-to-date overview of these current cardiac troponin research topics with their potential clinical implications. Typical clinical cases illustrate how to interpret cTn in the individual patient and how to derive a correct diagnosis.
当前的常规高敏心肌肌钙蛋白检测因其高分析灵敏度和特异性，是实验室诊断心肌损伤的标准。然而，在日常临床实践中，与以往几代心肌肌钙蛋白检测相比，心肌肌钙蛋白检测结果意外升高且无明显临床关联的情况越来越常见。在这些患者中，包括心脏磁共振成像在内的影像学技术有时可能无法检测到心肌损伤。这引发了人们对心肌肌钙蛋白释放病理生理学的更多关注，特别是肌钙蛋白是否能在无心肌坏死的情况下释放，从而导致全身循环中心肌肌钙蛋白升高。尽管有体外证据表明心脏生物标志物可从可逆性损伤的培养心肌细胞中释放，但在动物实验中，除了不同形式的细胞死亡（即凋亡或坏死）外，仍缺乏心肌肌钙蛋白释放的证据。相反，使用不同分析方法在人类血液样本中已鉴定出多种循环心肌肌钙蛋白形式，这就提出了一个问题，即通过测量特定循环心肌肌钙蛋白形式能否可靠地确定心肌损伤的原因。初步临床数据表明，检测特定循环肌钙蛋白形式可提高心肌肌钙蛋白诊断急性冠状动脉综合征所致急性心肌梗死的特异性。本综述旨在提供这些当前心肌肌钙蛋白研究主题及其潜在临床意义的最新概述。典型临床病例说明了如何在个体患者中解读心肌肌钙蛋白以及如何得出正确诊断。
