According to other studies,6,7 these patients presented a progressive decline in PaO2/FiO2 ratio (Figure 1B) and low compliance levels during hospitalization (Supporting information Table S5), suggesting a poor clinical outcome. ...fibrotic phenotype patients showed neutrophil extracellular traps to a significantly greater extent throughout lung parenchyma compared to thrombotic phenotype patients (p = 0.0004) (Supporting information Figure S3), which is a crucial response during the acute COVID-19 phase and a potential contributory factor to later fibrotic phase by amplifying the chronic reparative phase.8 IMAGE OMITTED. ...sudden death occurred, probably due to higher frequency (80%) of pulmonary thromboembolism (Supporting information Table S6), equally described in other study.10 As expected, d-dimer levels and platelet counts were higher in these patients than in fibrotic phenotype subjects (Supporting information Figure S1A and B and Table S8). ...the longer disease progression could give histopathological basis for an organizing phase, with sustained myofibroblastic proliferation, interstitial scarring and parenchymal remodeling, representing the “birth” of fibrosis as a future and possible sequel in post-COVID-19 patients, called as the fibrotic phenotype; or gradual recovery of the acute/sub-acute lung injury associated with thrombosis and unexpected sudden death, called as thrombotic phenotype (Figures 1 and 3). ...we believe that the categorization of patients based on these two phenotypes can be used to develop prognostic tools and potential therapies since the PaO2/FiO2 ratio and d-dimer correlate with the underlying fibrotic or thrombotic pathophysiologic process, which may indicate the possible clinical outcome of the patient.