Associations between hemostatic markers and mortality in COVID-19 – Compounding effects of D-dimer, antithrombin and PAP complex

The temporal changes of hemostatic activity in hospitalized patients with COVID-19: a prospective observational study

“…We believe that increased concentrations of potent fibrinolysis inhibitors (α2AP and PAI-1) outweighed increased levels of tPA and shifted the balance towards hypofibrinolysis. [23,24] Finally, increased vWF:Ag, PAI-1and particularly high vWF:Ag/ADAMTS-13 ratio suggest significant endothelial dysfunction and significant deviations in the ADAMTS13-von Willebrand factor axis [15,[25][26][27]. Presented results corroborate previous reports in terms of observed abnormalities and confirm their association with severity of COVID-19.…”

Dysregulated miRNAs network in the critical COVID-19: An important clue for uncontrolled immunothrombosis/thromboinflammation

“…1 D). The elevated levels and activity of several markers related to the ECs activation/dysfunction and pyroptosis ( e.g ., VWF, P-selectin, intercellular adhesion molecule 1 (ICAM-I), vascular cell adhesion molecule 1 (VCAM-1), and caspase-1) were observed in the patients with the critical COVID-19 positively associated with the disease severity and mortality [102] , [117] , [119] , [128] , [129] , [130] , [131] . Known as a stimulator of coagulation, complement activation, and NETosis, the VWF plays a major role in the uncontrolled immunothrombosis [132] , [133] ( Fig.…”

Role of Fibrinolysis in the Management of Patients with COVID-19 and Thromboembolic Complications: A Review

“…An impaired fibrinolytic process has been demonstrated in patients infected with SARS-CoV-2 with interstitial lung disease, including critically ill patients [ 8 , 9 , 10 ]. Hypercoagulation in these patients is a complex and multifactorial process.…”

“…It is considered that with SARS-CoV-2 virus attachment, excess angiotensin increases the expression of PAI-1, which inhibits fibrinolysis on endothelial cells [ 3 , 11 ]. Patients with interstitial lung disease were also reported to have elevated levels of thrombin-activatable fibrinolysis inhibitor and protein C inhibitor (plasminogen activator inhibitor-3) [ 9 ]. SARS-CoV-2 infection leads to acute inflammation, which leads to an increase in bradykinin and tPA.…”

“…However, increased tPA levels are not sufficient to counterbalance the high levels of PAI-1, which likely explains the impaired fibrinolysis and fibrin accumulation in the lung alveoli [ 12 ]. Fibrin deposits enhance inflammation and fibrosis, and lead to lung surfactant damage [ 9 ].…”