Clinicopathological factors potentially relevant to pulmonary intravascular fibrin organisation in patients with COVID-19: an autopsy-based study.

Microvascular thrombosis is a hallmark of severe COVID-19, but the structural organisation of fibrin within these thrombotic formations remains poorly characterized. We previously identified a distinctive radial fibrin pattern in pulmonary and renal microvessels; however, factors potentially relevant to its formation were not explored. The objective of this study was to identify clinicopathological variables potentially relevant to the formation of the radial fibrin pattern. In a retrospective observational cohort of 307 patients with COVID-19, clinical and laboratory parameters were compared between survivors and non-survivors to contextualize findings in a subset of 40 autopsied patients. Within this autopsied subset, cases were stratified according to the presence and architecture of intravascular fibrin. Clinical and laboratory parameters were evaluated across groups, and immunohistochemical studies were performed to detect platelets and endothelial-associated factors within intravascular fibrin. The radial pattern of intravascular fibrin was observed in areas of severe tissue injury. Immunohistochemistry demonstrated CD61-positive platelets within these structures, with Factor VIII and von Willebrand factor positivity. Cases with a radial pattern of intravascular fibrin showed significantly lower calcium levels and higher procalcitonin concentrations, together with trends toward increased inflammatory and coagulation markers, consistent with the broader cohort analysis in which nonsurvivors exhibited higher inflammatory and coagulation parameters. These findings suggest that, in severe COVID-19, intravascular fibrin with a radial pattern may arise in a hypercoagulable setting marked by systemic inflammation, in which hypocalcaemia appears to be a relevant variable.