Abstract
High rates of thrombosis are present in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Deeper insight into the prothrombotic state is essential to provide the best thromboprophylaxis care. Here, we aimed to explore associations among platelet indices, conventional hemostasis parameters, and viscoelastometry data. This pilot study included patients with severe COVID-19 (n = 21) and age-matched controls (n = 21). Each patient received 100 mg aspirin therapy at the time of blood sampling. Total platelet count, high immature platelet fraction (H-IPF), fibrinogen, D-dimer, Activated Partial Thromboplastin Time, von Willebrand factor antigen and von Willebrand factor ristocetin cofactor activity, plasminogen, and alpha2-antiplasmin were measured. To monitor the aspirin therapy, a platelet function test from hirudin anticoagulated whole blood was performed using the ASPI test by Multiplate analyser. High on-aspirin platelet reactivity (n = 8) was defined with an AUC > 40 cut-off value by ASPI tests. In addition, in vitro viscoelastometric tests were carried out using a ClotPro analyser in COVID-associated thromboembolic events (n = 8) (p = 0.071) nor the survival rate (p = 0.854) showed associations with high on-aspirin platelet reactivity status. The platelet count (p = 0.03), all subjects. COVID-19 patients presented with higher levels of inflammatory markers, compared with the controls, along with evidence of hypercoagulability by ClotPro. H-IPF (%) was significantly higher among non-survivors (n = 18) compared to survivors (p = 0.011), and a negative correlation (p = 0.002) was found between H-IPF and plasminogen level in the total population. The platelet count was significantly higher among patients with high on-aspirin platelet reactivity (p = 0.03). Neither the ECA-A10 (p = 0.008), and ECA-MCF (p = 0.016) were significantly higher, while the tPA-CFT (p < 0.001) was significantly lower among patients with high on-aspirin platelet reactivity. However, only fibrinogen proved to be an independent predictor of hypofibrinolysis in severe COVID-19 patients. In conclusion, a faster developing, more solid clot formation was observed in aspirin ‘non-responder’ COVID-19 patients. Therefore, an individually tailored thromboprophylaxis is needed to prevent thrombotic complications, particularly in the hypofibrinolytic cluster.
Highlights
The COVID-19 pandemic, caused by SARS-CoV-2, is a contagious potentially lifethreatening disease that has caused more than five million deaths worldwide [1]
Clinical characteristics of the disease can range from mild upper tract respiratory infection to multiple organ disfunction (MODS), multiple organ failure (MOF), and fatal hypoxemic respiratory failure [2,3]
Welder et al found that percentfound be at predictive of the fatal outcome
Summary
The COVID-19 pandemic, caused by SARS-CoV-2, is a contagious potentially lifethreatening disease that has caused more than five million deaths worldwide [1]. Clinical characteristics of the disease can range from mild upper tract respiratory infection to multiple organ disfunction (MODS), multiple organ failure (MOF), and fatal hypoxemic respiratory failure [2,3]. There is a great body of evidence that COVID-19 significantly affects the coagulation system, contributing to hypercoagulable states and thrombotic events. The reason for such alterations is multifactorial, including the activation of the thrombo-inflammatory cascade and endothelial dysfunction [4,5]. There is a great need to identify novel markers to stratify disease severity and predict the outcome of disease
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