Cardiac inflammation in COVID-19: Lessons from heart failure

Life Sci. 2020 Nov 1:260:118482. doi: 10.1016/j.lfs.2020.118482. Epub 2020 Sep 21.


Cardiovascular disease (CVD) is the most common co-morbidity associated with COVID-19 and the fatality rate in COVID-19 patients with CVD is higher compared to other comorbidities, such as hypertension and diabetes. Preliminary data suggest that COVID-19 may also cause or worsen cardiac injury in infected patients through multiple mechanisms such as 'cytokine storm', endotheliosis, thrombosis, lymphocytopenia etc. Autopsies of COVID-19 patients reveal an infiltration of inflammatory mononuclear cells in the myocardium, confirming the role of the immune system in mediating cardiovascular damage in response to COVID-19 infection and also suggesting potential causal mechanisms for the development of new cardiac pathologies and/or exacerbation of underlying CVDs in infected patients. In this review, we discuss the potential underlying molecular mechanisms that drive COVID-19-mediated cardiac damage, as well as the short term and expected long-term cardiovascular ramifications of COVID-19 infection in patients.

Keywords: COVID-19; Cytokine storm; Heart failure; Immunopathology; Macrophages; Monocytes; Myocarditis; Myofibroblasts; Neutrophils; SARS-Cov2.

Publication types

  • Review

MeSH terms

  • Betacoronavirus / isolation & purification*
  • COVID-19
  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / pathology
  • Coronavirus Infections / complications*
  • Coronavirus Infections / transmission
  • Coronavirus Infections / virology
  • Humans
  • Inflammation / etiology*
  • Inflammation / pathology
  • Pandemics
  • Pneumonia, Viral / complications*
  • Pneumonia, Viral / transmission
  • Pneumonia, Viral / virology
  • Prognosis
  • SARS-CoV-2