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    Poster Networking

    COVID

    Poster Networking Session

    PB0064 - Involvement of platelet activation in Long COVID-19 Syndrome

    Sunday, June 25, 2023
    18:30 – 19:30 ET
    Room: Exhibition
    Background: Long-COVID-19 syndrome (LCS) is defined as symptoms persisting after remission of acute infection. We documented that in acute COVID-19 patients platelets are activated and show a prothrombotic phenotype. It is currently unknown whether this phenotype can sustain the residual pulmonary impairment observed in LCS patients.

    Aims: To characterize the persistence of platelet activation and prothrombotic phenotype 6-months after acute COVID-19 syndrome remission in LCS patients.

    Methods: 66 patients with a 6-month follow-up (FU) post SARS-CoV-2 infection were enrolled. 25/66 subjects (38%) referred 2 or more symptoms suggestive of LCS (memory loss: 80%, dyspnea: 64%, recurrent fatigue: 64%). Platelet activation (P-selectin, Tissue Factor [TF] and platelet-leukocyte aggregates [PLA]) and microvesicle (MV) profile were analyzed by flow cytometry while platelet thrombin generation capacity (pTGC) was assessed by calibrated automated thrombogram. Cardiopulmonary Exercise Testing (CPET) and pulmonary 64-rows-CT scan evaluation were performed. 46 patients enrolled during acute COVID-19 infection and 46 healthy subjects (HS) were used for comparison.

    Results: TFpos-platelet and TFpos -MV levels were 3- and 2-fold lower at FU compared to acute phase, being similar to HS. Also pTGC and MV profile returned to physiological levels. Conversely, a 2.5-fold higher P-selectin expression and PLA formation was observed at FU compared to HS. Interestingly, in LCS patients, PLA were 1.5-fold higher than in asymptomatic FU patients and were significantly associated with lung volume failure (r=0.51, p=0.04). No correlation was found in asymptomatic FU patients. In ex vivo experiments, plasma of LCS patients induced platelet P-selectin expression and PLA formation, features reverted by aspirin and P2Y12 inhibitor treatment.

    Conclusion(s): These data suggest that: 1) the presence of PLA in the bloodstream may contribute to pulmonary dysfunction still observed in LCS patients; 2) the potential benefit of antiplatelet agents in the resolution of platelet activation in LCS patients.