4.7 Article

COVID-19-related cardiac complications from clinical evidences to basic mechanisms: opinion paper of the ESC Working Group on Cellular Biology of the Heart

Journal

CARDIOVASCULAR RESEARCH
Volume 117, Issue 10, Pages 2148-2160

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvab201

Keywords

SARS-CoV-2; COVID-19; Myocardial injury; Disease modelling; Infection; Inflammation

Funding

  1. Italian Ministry of Health (Ricerca Corrente)
  2. Lombardy Region (POR FESR 2014-2020-LINEA 2A COVID) [1850333]
  3. National Research, Development and Innovation Office of Hungary (Research Excellence Program-TKP)
  4. National Research, Development and Innovation Office of Hungary (National Heart Program) [NVKP 16-1-2016-0017]
  5. National Research, Development and Innovation Office of Hungary (Investment Into The Future-Covid19 projects at Semmelweis University)
  6. Higher Education Institutional Excellence Program of the Ministry of Human Capacities in Hungary
  7. EU Horizon 2020 project COVIRNA [101016072]
  8. EU Horizon 2020 project CRYSTAL3 (MSCA-RISE Project) [101007931]
  9. Incyte
  10. Ministero dell'Istruzione, Universita e Ricerca Scientifica [549901_2020_Madonna: Ateneo]
  11. Horizon2020 ERC-2016-COG EVICARE [725229]
  12. Horizon 2020 BRAV3 [SC1-BHC-07-2019]
  13. Dutch Heart Foundation (DnAFiX project) [2020B003]
  14. AFFIP [CVONSTW2016-14728]
  15. European Research Council (ERC) [725229] Funding Source: European Research Council (ERC)

Ask authors/readers for more resources

The COVID-19 pandemic poses a potential threat to the heart, especially in elderly individuals. In addition to immediate damage, long-term consequences could increase the risk of cardiac complications. Further research is needed to fully understand the mechanisms of cardiac injury in COVID-19.
The pandemic of coronavirus disease (COVID)-19 is a global threat, causing high mortality, especially in the elderly. The main symptoms and the primary cause of death are related to interstitial pneumonia. Viral entry also into myocardial cells mainly via the angiotensin converting enzyme type 2 (ACE2) receptor and excessive production of pro-inflammatory cytokines, however, also make the heart susceptible to injury. In addition to the immediate damage caused by the acute inflammatory response, the heart may also suffer from long-term consequences of COVID-19, potentially causing a post-pandemic increase in cardiac complications. Although the main cause of cardiac damage in COVID-19 remains coagulopathy with micro- (and to a lesser extent macro-) vascular occlusion, open questions remain about other possible modalities of cardiac dysfunction, such as direct infection of myocardial cells, effects of cytokines storm, and mechanisms related to enhanced coagulopathy. In this opinion paper, we focus on these lesser appreciated possibilities and propose experimental approaches that could provide a more comprehensive understanding of the cellular and molecular bases of cardiac injury in COVID-19 patients. We first discuss approaches to characterize cardiac damage caused by possible direct viral infection of cardiac cells, followed by formulating hypotheses on how to reproduce and investigate the hyperinflammatory and pro-thrombotic conditions observed in the heart of COVID-19 patients using experimental in vitro systems. Finally, we elaborate on strategies to discover novel pathology biomarkers using omics platforms.

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