Department of Cardiovascular Diseases, Mayo Clinic, 200 1st Street Southwest, Rochester, MN 55905, USA; Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Via Giustiniani 2, Padova 35128, Italy.
Department of Cardiovascular Diseases, Mayo Clinic, 200 1st Street Southwest, Rochester, MN 55905, USA; Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 1st Street Southwest, Rochester, MN 55905, USA.
Cardiol Clin. 2022 Aug;40(3):287-300. doi: 10.1016/j.ccl.2022.03.005. Epub 2022 Mar 31.
Myocardial injury is common in patients with COVID-19 and is associated with an adverse prognosis. Cardiac troponin (cTn) is used to detect myocardial injury and assist with risk stratification in this population. SARS-CoV-2 infection can play a role in the pathogenesis of acute myocardial injury due to both direct and indirect damage to the cardiovascular system. Despite the initial concerns about an increased incidence of acute myocardial infarction (MI), most cTn increases are related to chronic myocardial injury due to comorbidities and/or acute nonischemic myocardial injury. This review will discuss the latest findings on this topic.
心肌损伤在 COVID-19 患者中很常见，并且与不良预后相关。心肌肌钙蛋白（cTn）用于检测心肌损伤，并协助该人群进行风险分层。SARS-CoV-2 感染可通过直接和间接损伤心血管系统在急性心肌损伤的发病机制中发挥作用。尽管最初担心急性心肌梗死（MI）的发生率增加，但大多数 cTn 升高与合并症和/或急性非缺血性心肌损伤引起的慢性心肌损伤有关。这篇综述将讨论该主题的最新发现。
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