Pulmonary Thrombosis in Patients With COVID-19 Pneumonia. Is It Really a True Pulmonary Thromboembolism?

Abstract

Background Mechanisms of pulmonary thrombosis (PT) in COVID-19 are unknown. Thromboembolism and local pulmonary inflammation have been suggested as the main factors. However, robust evidence is still lacking because this was mainly based on retrospective studies, in which patients were included when PT was suspected. On the other hand, the number of thrombi within lung opacification, and the association with percentage of pulmonary involvement (TLI) related to COVID-19 were not evaluated. The main objective was to determine the number and percentage of thrombi surrounded by lung opacification (TSO) in each patient, as well as their relationship with TLI. Methods Consecutive patients with COVID-19 pneumonia performed computed tomography pulmonary angiography. We determined TLI and TSO in patients with PT. TLI was automatically calculated by artificial intelligence analysis. TSO was defined when there was lung opacification ≤ 10 mm from each pulmonary vessel with a thrombus. Analyses at patient level (TLI and percentage of TSO) and at thrombi level (TLI and TSO) were performed. Results We diagnosed PT in 70 out of 184 patients. Three (2–8) thrombi/patient were detected. The median percentage of TSO was 100% per patient (75–100%), and TLI was 19.9% (4.6–35.2) in all patients. Sixty-five patients (92.9%) were above the random scenario (in which the percentage of TSO should correspond to the percentage of lung involvement in each patient), and had more percentage of TSO than TLI in each patient. Most thrombi (n = 299, 75.1%) were TSO. When evaluating by TLI (< 10%, 10–20%, 20–30%, and > 30%), percentage of TSO was higher in most groups. Thrombi were mainly in subsegmental/segmental arteries, and percentage of TSO was higher in all locations. Conclusion Thrombi in COVID-19 pneumonia complicated with PT were found within lung opacities in a higher percentage than lung involvement, regardless of the proportion of pulmonary infiltrates and clot location, supporting the hypothesis that COVID-19 could promote local pro-thrombotic phenomena rather than “classic thrombo-embolism”. These data expand understanding of PT in COVID-19 and support a partial justification for why thromboprophylaxis does not prevent PT. Further studies should focus on new strategies to reduce the thrombotic risk.