Background
Cardiac injury (CI) in COVID-19 is associated with worse clinical outcomes but its mechanism remains unclear. Direct viral myocardial infiltration has not been widely demonstrated. We sought to better understand the mechanism of CI in hospitalized patients with COVID-19.
Methods
We collected plasma from 49 hospitalized COVID-19 patients, among whom 17 had CI defined by troponin T (TnT) level ≥ 0.01. Multiplex profiling of 100+ factors (Eve Tech., Calgary, Canada) associated with: 1) immune activation, 2) angiogenesis, 3) obesity, and 4) thrombosis was conducted. We rank-ordered the factors based on their importance in predicting elevated TnT.
Results
We found that increased levels of resistin, LCN2, and HGF, markers of neutrophil activation (NA), and decreased ADAMTS13/Von Willebrand factor (A13/VWF) ratio, a marker of pro-thrombotic state, were significant ranking factors correlated with TnT. Moreover, cardiac staining found evidence of neutrophil driven NETosis in hearts of COVID-19 patients. Circulating levels of resistin, LCN2, HGF, and A13/VWF ratio were significantly correlated with TnT. There was a significant inverse correlation between NA and A13/VWF ratio.
Conclusion
Our findings support a pro-thrombotic milieu from increased NA and decreased A13/VWF ratio as a critical driver of CI in COVID-19. NA may decrease the A13/VWF ratio and promote thrombosis. These data should generate hypothesis for cardio-protective therapies in COVID-19.
Footnotes
Poster Contributions
Monday, May 17, 2021, 12:15 p.m.-1:00 p.m.
Session Title: Spotlight on Special Topics: COVID 8
Abstract Category: 61. Spotlight on Special Topics: Coronavirus Disease (COVID-19)