Platelets and COVID-19: Inflammation, Hyperactivation and Additional Questions

UMMS Affiliation

Department of Medicine, Division of Cardiovascular Medicine

Publication Date


Document Type



Biological Factors | Cardiovascular Diseases | Cardiovascular System | Hemic and Immune Systems | Immunology and Infectious Disease | Infectious Disease | Microbiology | Pathological Conditions, Signs and Symptoms | Virus Diseases


The mechanisms underlining thrombosis in COVID-19 patients are not known and likely due to multiple processes including inflammation, oxygen demand injury, and plaque rupture triggered by the infection. Platelets mediate thrombotic vascular occlusion but are also increasingly recognized to have immunomodulatory activity. Several of our recent studies have characterized the role of viral infections in cardiac disease. Although robust data on the scope of acute myocardial infarction in COVID-19 are not yet available, myocardial infarction contributed to in-hospital mortality during previous severe acute respiratory syndrome/coronavirus epidemics. A recent study has also demonstrated that influenza and other respiratory viruses increase the incidence of acute myocardial infarction particularly in the first 7 days post-infection, suggesting that platelets may be directly involved in mediating an immune response but, when dysregulated, can also lead to thrombotic vascular occlusion.


thrombosis, COVID-19, platelets, inflammation, UMCCTS funding

DOI of Published Version



Koupenova M, Freedman JE. Platelets and COVID-19: Inflammation, Hyperactivation and Additional Questions. Circ Res. 2020 Nov 6;127(11):1419-1421. doi: 10.1161/CIRCRESAHA.120.318218. Epub 2020 Nov 5. PMID: 33151798; PMCID: PMC7641185. Link to article on publisher's site

Journal/Book/Conference Title

Circulation research

Related Resources

Link to Article in PubMed

PubMed ID