COVID-19 is known for its highly (pro)thrombotic events following SARS-CoV-2 infection. Ultimately, disruption of the vasculature results in multiple organ failure and long-term COVID-19 related cardiorespiratory damage. While both host immunity and inflammatory and pathogenic features of this SARS-Coronavirus contribute to vascular injury, it is the virus that is the cause of the thromboinflammatory state that characterizes COVID-19. In the following slides, I will describe the mechanisms underlying thrombotic events in COVID-19 patients.
 |
| Markers to assess the thromboinflammatory state of COVID-19 patients |
 |
| Thrombocyopenia in COVID-19: while values are normal at the time of hospital admission, thrombocytopenia appears as a progressive feature |
 |
| Dysregulation of thrombin and fibrin in COVID-19 |
 |
| Urokinase pathway involvement in COVID-19 thrombosis |
