Cardiovascular comorbidities, myocardial injury and repurposed drugs in COVID-19 disease*

J.M. Leerink

Department of Clinical and Experimental Cardiology, Heart Centre, Amsterdam UMC, Location Academic Medical Center, Amsterdam, The Netherlands

*Weergave van bespreking tijdens Journal Club meeting van de afdelingen cardiologie van Amsterdam UMC en OLVG d.d. 26 maart 2020

Presentation on Clerkin et al. 2020, Circulation, Coronavirus Disease 2019 (COVID-19) and Cardiovascular Disease.

This review article discusses the current evidence on COVID-19 and cardiovascular disease.

The SARS-COV-2 virus that causes COVID-19 disease mainly infects lower respiratory cells through the ACE2 receptor causing mostly respiratory symptoms. However, it is now known that cardiovascular comorbidities are common in COVID-19 patients and are more common in those with more severe disease. This increased risk may be mediated trough an older age, immune system impairments or through increased ACE2 receptor expression in patients with cardiovascular disease.

Elevated troponins are reported in 7% of the hospitalized patients and 22% of the critically ill patients. Two patterns of myocardial injury are observed in COVID-19 disease: 1) troponin elevations associated with cytokine storm in the critically ill and 2) direct myocardial injury through virus entry via the ACE2 receptor that is also expressed on cardiomyocytes.

Direct myocardial infection is further supported by autopsy studies with SARS-COV virus RNA present in 35% of the autopsied hearts.

While we wait for vaccines, numerous repurposed drugs are currently under investigation for treatment of COVID-19 disease (Table 1.)

Table 1. Repurposed drugs under investigation for COVID-19 disease:

Drug Original indication(s) Mode of action Early outcomes in COVID-19
Recombinant ACE2 (APN01) ARDS Decrease angiotension II and IL6, virus neutralization X
-Camostat mesylate Pancreatitis, oesophagitis Block TMPRSS2 activity and virus entrance via spike protein X
Remdesevir Ebola Blocks RNA replication In vitro activity against SARS-CoV-2
Chloroquine, Hydroxychloroquine Malaria, RA, SLE Block SARS-CoV-2 entry Pneumonia severity, shorter hospitalization, and earlier viral clearance


HIV, SARS Protease inhibitor Negative RCT in 199 patients
Favipiravir Influenza Inhibits RNA replication X
Tocilizumab, Sarilumab RA, cytokine release syndrome IL-6 receptor antagonist Trials ongoing in COVID-19 with cytokine storm