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Individuals who were asymptomatic and underwent PET/CT within a period of 1–180 days following their second vaccination exhibited increased myocardial 18Fluorine-fluorodeoxyglucose uptake as compared to unvaccinated individuals.
The S1 subunit of the SARS-CoV-2 spike protein induces endothelial inflammation via ACE2 through processes that are independent of viral replication.
This study showed that SARS-CoV-2 infected macrophages in coronary atherosclerotic lesions, resulting in plaque inflammation that may promote acute cardiovascular complications.
The retrospective pharmacovigilance study with a comprehensive analysis of potential safety signals associated with myocarditis/pericarditis after the primary and up to three booster doses of mRNA anti-SARS-CoV-2 vaccines in different age groups.
Impaired systolic and diastolic myocardial deformation and the persistent late gadolinium enhancement were found in a significant subset of patients.
The findings showed that myocardial injury after mRNA-1273 booster vaccination occurred in one out of 35 people (2.8%), which was higher than incidence estimated in meta-analyses of hospitalized cases with myocarditis (incidence of 0.0035%) after the second vaccination.
Cardiac MRI revealed signs of non-ischemic myocardial fibrosis in in 30% of PASC/long COVID patients, exceeding the prevalence in the normal adult population.
The cytokinopathy and profibrotic myeloid cell response suggest cytokine-dependent pathology possibly associated with myeloid cell–associated cardiac fibrosis in myocarditis after mRNA SARS-CoV-2 vaccination.
PET and MRI visualization of myocardial tissue showed that localized myocardial inflammation and edema is present in a small proportion of patients with symptomatic myocarditis at approximately 2 months after anti-SARS-CoV-2 vaccination.
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Results showed that the overall risk of all forms of retinal vascular occlusion was 2.19 times higher in the vaccinated cohort than in the unvaccinated cohort in the 2 years after vaccination.
These findings revealed the possibility that autoimmunity to desmoglein 2 contributes to cardiac sequelae associated with C-19 infection.
SARS-CoV-2 S1 subunit of the spike (S) protein by itself promotes cell signaling in the vasculature. A morphometric analysis of the pulmonary vessels showed wall thickness in patients who died of SARS-CoV-2.
Adolescents and young adults with myocarditis after SARS-CoV-2 mRNA vaccination had significantly higher levels of free full-length spike protein in their plasma, whereas asymptomatic vaccinated control subjects had no detectable free spike protein.