• Guozhi Xia, Di Fan, Chaoran Ma, Yanru He, Ming Wang, Yaowu Zhu, and Qiangsun Zheng.
• Department of Cardiology, Second Affiliated Hospital of Xi'an Jiaotong University, No. 157 West 5th Road, Xi'an 710004, Shaanxi, China. Electronic address: hatozy@126.com.
• Am. J. Med. Sci. 2021 Jun 1; 361 (6): 718-724.

BackgroundInflammation can facilitate development of coronavirus disease 2019 (COVID-19) and cardiac injury is associated with worse clinical outcomes. However, data are relatively scarce on the association between hyper-inflammatory response and cardiac injury among COVID-19 patients.MethodsThe study was designed based on severe and critically ill patients with COVID-19. Information on clinical characteristics and laboratory examinations was collected from the electronic medical records and analyzed.ResultsThere were 32.4% (n = 107) of patients with cardiac injury. The median age was 67 years, and 48.8% (n = 161) of patients were men. Hypertension was the most common in 161 (48.8%) patients, followed by diabetes (16.7%, n = 55) and coronary heart disease (13.3%, n = 44). Compared to cases without cardiac injury, those with cardiac injury were older, had higher proportions of coronary heart disease, and leukocyte counts, significantly elevated concentrations of N-terminal pro-B-Type natriuretic peptide, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-α, interleukin-2 receptor (IL-2R), IL-6, and IL-8, but lower lymphocyte counts. A significant positive correlation was observed between high-sensitivity troponin I and inflammatory cytokines. Logistic regression analysis showed that hs-CRP, TNF-α and IL-6 were independent risk factors for cardiac injury.ConclusionsCardiac injury was associated with elevated levels of inflammatory cytokines among severe and critically ill patients with COVID-19, suggesting that hyper-inflammatory response may involve in cardiac injury.Copyright © 2021 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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