Table 2.
Findings of cardiovascular disease, myocarditis, and infection
| Findings | Studies | |
|---|---|---|
| SARS-CoV-2 viral access to heart | RNAaemia in only six (15%) of 41 COVID-19 cases; cardiac injury linked to intensive care unit admission and not RNAaemia | Huang at al3 |
| Community-acquired pneumonia and bronchopneumonia | Increased risk of cardiovascular death | Smeeth et al,17 Corrales-Medina et al18 |
| Human cardiac myocytes | No cytopathic change with SARS; no SARS viral protein detection | Hwang et al19 |
| Viral myocarditis | 47 cases of fatal influenza virus; fatalities predominantly in children and women; myocarditis deemed to be cause of death in five cases | Guarner et al20 |
| Cardiac injury not specific to COVID-19 | Cardiac injury in >60% with avian influenza H7N9 infection suggesting that cardiac disease linked to infection; also linked to history of cardiovascular disease, but not male sex or diabetes (myocarditis is well documented with influenza) | Gao et al34 |
| Cardiac injury not specific to COVID-19 | Pandemic (H1N1) 2009 virus; cardiac injury in 46% of cases; mean age 34 years; more common in women than in men; presumed myocarditis (no histology or post-mortem data) | Chacko et al35 |
| COVID-19 viral access to heart | No viraemia in nine cases of COVID-19 | Wölfel et al36 |
| Endothelial cells | Express ACE2 but cytopathic changes seen in pneumocytes not reported | Oudit et al37 |
| Other factors linked to cardiac pathology | Older age, male sex, hypertension, obesity, diabetes; hypoxia from acute respiratory distress syndrome development; emergent disseminated intravascular coagulation late in COVID-19 disease course | Guzik et al38 |
| Viral myocarditis | H1N1 influenza A virus; rare link to fulminant myocarditis reported | Bratincsák et al39 |
SARS-CoV-2=severe acute respiratory syndrome coronavirus 2. COVID-19=coronavirus disease 2019. SARS=severe acute respiratory syndrome. ACE2=angiotensin-converting enzyme 2.