The pathophysiology of COVID-19-associated coagulopathy is complex and not fully understood. SARS-CoV-2 spike protein (SP) may activate platelets and interacts with fibrin(ogen). We aimed to investigate the possible evidence of isolated SP in clots retrieved in COVID-19 patients with acute ischemic stroke (by mechanical thrombectomy) and myocardial infarction.
In this pilot study we could detect SP, but not nucleocapsid protein, on platelets of COVID-19 + patients’ thrombi. In addition, in all the three COVID-19 + thrombi analyzed for molecular biology, no SARS-CoV-2 RNA could be detected by real time-polymerase chain reaction. These data confirm the hypothesis that free SP besides the whole virus, may be the trigger of platelet activation and clot formation in COVID-19.