Myocardial and Vascular Involvement in COVID-19 and Post-Vaccination States: Understanding Injury Pathways and Clinical Implications
Roxana-Nicoleta Siliste, Serban Benea, Corina Homentcovschi, Teodora Deaconu, Constantin Caruntu, Ilinca Savulescu-Fiedler

TL;DR
This paper explores how SARS-CoV-2 infection and vaccination can cause heart and blood vessel injuries, comparing their mechanisms and clinical outcomes.
Contribution
The paper provides a synthesis of recent evidence on myocardial and vascular injury mechanisms in both COVID-19 and post-vaccination states.
Findings
Myocardial injury in COVID-19 involves direct viral effects and immune-mediated inflammation.
Vaccine-associated myocarditis is likely due to immune-related mechanisms and is generally self-limiting.
The risk of myocarditis from vaccination is much lower than from SARS-CoV-2 infection.
Abstract
Myocardial and vascular injury secondary to SARS-CoV-2 infection and vaccination has emerged as a clinically relevant phenomenon, with distinct but overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral effects and immune-mediated inflammation, supported by histopathological studies revealing macrophage-rich infiltrates, microthrombosis, and supporting fibrosis in isolated areas. In contrast, vaccine-associated myocarditis—reported predominantly following mRNA vaccines—has a self-limiting clinical course, with mechanisms likely involving molecular mimicry, aberrant immune activation, or hypersensitivity reactions, although these pathways require further validation. Although mRNA vaccines have been associated with a small increase in myocarditis, particularly in young men, the risk is significantly lower than that associated with…
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Taxonomy
TopicsSARS-CoV-2 and COVID-19 Research · Heparin-Induced Thrombocytopenia and Thrombosis · COVID-19 Clinical Research Studies
