Solaro R John, Rosas Paola C, Langa Paulina, Warren Chad M, Wolska Beata M, Goldspink Paul H
Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL, USA.
Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL, USA.
Int J Cardiol Cardiovasc Dis. 2021;1(2):41-47. doi: 10.46439/cardiology.1.006. Epub 2021 Mar 8.
Serum levels of thin filament proteins, cardiac troponin T (cTnT) and cardiac troponin I (cTnI) employing high sensitivity antibodies provide a state-of-the art determination of cardiac myocyte injury in COVID-19 patients. Although there is now sufficient evidence of the value of these determinations in patients infected with SARS-CoV-2, mechanisms of their release have not been considered in depth. We summarize the importance of these mechanisms with emphasis on their relation to prognosis, stratification, and treatment of COVID-19 patients. Apart from frank necrotic cell death, there are other mechanisms of myocyte injury leading to membrane fragility that provoke release of cTnT and cTnI. We discuss a rationale for understanding these mechanisms in COVID-19 patients with co-morbidities associated with myocyte injury such as heart failure, hypertension, arrythmias, diabetes, and inflammation. We describe how understanding these significant aspects of these mechanisms in the promotion of angiotensin signaling by SARS-CoV-2 can affect treatment options in the context of individualized therapies. Moreover, with likely omic data related to serum troponins and with the identification of elevations of serum troponins now more broadly detected employing high sensitivity antibodies, we think it is important to consider molecular mechanisms of elevations in serum troponin as an element in clinical decisions and as a critical aspect of development of new therapies.
使用高灵敏度抗体检测血清中细肌丝蛋白、心肌肌钙蛋白T（cTnT）和心肌肌钙蛋白I（cTnI）的水平，可为新冠病毒肺炎（COVID-19）患者的心肌细胞损伤提供最先进的检测方法。尽管目前已有充分证据表明这些检测方法对感染严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的患者具有重要价值，但其释放机制尚未得到深入研究。我们总结了这些机制的重要性，重点强调了它们与COVID-19患者预后、分层和治疗的关系。除了明显的坏死性细胞死亡外，还有其他导致心肌细胞损伤的机制，这些机制会导致细胞膜脆弱，从而引发cTnT和cTnI的释放。我们讨论了在患有与心肌细胞损伤相关的合并症（如心力衰竭、高血压、心律失常、糖尿病和炎症）的COVID-19患者中理解这些机制的基本原理。我们描述了了解这些机制在SARS-CoV-2促进血管紧张素信号传导中的重要方面如何在个体化治疗背景下影响治疗选择。此外，鉴于可能存在与血清肌钙蛋白相关的组学数据，以及现在使用高灵敏度抗体更广泛地检测到血清肌钙蛋白升高，我们认为将血清肌钙蛋白升高的分子机制作为临床决策的一个因素以及新疗法开发的关键方面来考虑非常重要。
