ABSTRACT
INTRODUCTION: Hemostatic abnormalities play an important role in the pathogenesis of COVID-19 and are considered to be determinants of patients` outcomes. Less is known about the dynamics of these abnormalities in a short-term observation. PATIENTS AND METHODS: This was a prospective observational study enrolling adult patients hospitalized due to COVID-19 in a tertiary centre in Poland from January to May 2021. Blood samples were drawn upon admission and 28 days after admission to measure markers of coagulation, fibrinolysis and endothelial dysfunction and to evaluate whether there are significant differences between these two time points. All analyses were performed in the entire cohort and after stratification into three groups depending on the degree of respiratory support. RESULTS: We recruited 245 patients at the median age of 63 years (IQR 52; 69), among whom 158 (64.5%) were males. Analysis of hemostatic markers on admission revealed hypercoagulability, hypofibrinolysis and endothelial dysfunction are related to degree of respiratory support. We found significant differences between the admission and 28-day follow-up in all markers except for plasminogen activity (123.75 vs. 121.60, p=0.938). Interestingly, markers of endothelial dysfunction remained the highest in the advanced respiratory support group after 28 days, while differences in other markers subsided. CONCLUSION: Hemostatic abnormalities are significantly attenuated within a month after hospital admission due to COVID-19. Initially observed association between severity of disease and hemostatic derangements persists only for markers of endotheliopathy.
ABSTRACT
BACKGROUND: Microclots, a term also used for amyloid fibrin(ogen) particles and henceforth named aggregates, have recently been reported in the plasma of patients with COVID-19 and long COVID. These aggregates have been implicated in the thrombotic complications of these diseases. METHODS: Plasma samples from 35 patients with acute pulmonary embolism were collected and analysed by laser scanning confocal microscopy and scanning electron microscopy before and after clotting. RESULTS: Here we confirm the presence of aggregates and show that they also occur in the plasma of patients with pulmonary embolism, both before and after clotting. Aggregates vary in size and consist of fibrin and platelets. We show that treatment with low-molecular weight heparin reduces aggregates in the samples of patients with pulmonary embolism. Double centrifugation of plasma does not eliminate the aggregates. CONCLUSIONS: These data corroborate the existence of microclots or aggregates in diseases associated with venous thromboembolism. Important questions are raised regarding their pathophysiological relevance and further studies are warranted to investigate whether they represent cause or consequence of clinical thrombosis.
When blood turns from liquid to solid, a protein called fibrin and cells called platelets aggregate to form a blood clot. Small aggregates have been found in the blood of people with COVID-19 and long COVID. Here, we show that small aggregates also occur in the blood of patients with pulmonary embolism, a disorder in which blood clots are trapped in an artery in the lung, preventing blood flow. We confirm that aggregates consist of fibrin and platelets, and show that the number of aggregates is lower when patients are treated with blood thinning drugs. These results suggest other disorders of the blood should also be investigated to see whether aggregates are present and whether they have an impact on the outcome for the patient. This could help us understand the cause of diseases associated with blood clotting, which might offer new approaches for diagnosis and treatment.