Increased left ventricular
fibrosis has been reported in patients hospitalized with
coronavirus disease 2019 (COVID-19). It is unclear whether this
fibrosis is a consequence of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2)
infection or a risk factor for severe
disease progression. We observed increased
fibrosis in the left ventricular myocardium of deceased
COVID-19 patients, compared with matched controls. We also detected increased
mRNA levels of soluble
interleukin-1 receptor-like 1 (sIL1-RL1) and
transforming growth factor β1 (TGF-β1) in the left ventricular myocardium of deceased
COVID-19 patients. Biochemical analysis of blood sampled from patients admitted to the emergency department (ED) with
COVID-19 revealed highly elevated levels of TGF-β1
mRNA in these patients compared to controls. Left ventricular strain measured by echocardiography as a marker of pre-existing cardiac
fibrosis correlated strongly with blood TGF-β1
mRNA levels and predicted disease severity in
COVID-19 patients. In the left ventricular myocardium and lungs of
COVID-19 patients, we found increased
neuropilin-1 (NRP-1)
RNA levels, which correlated strongly with the prevalence of pulmonary SARS-CoV-2 nucleocapsid. Cardiac and
pulmonary fibrosis may therefore predispose these patients to increased cellular viral entry in the lung, which may explain the worse clinical outcome observed in our cohort. Our study demonstrates that patients at risk of
clinical deterioration can be identified early by echocardiographic strain analysis and quantification of blood TGF-β1
mRNA performed at the time of first medical contact.