Mechanisms of late-onset thrombocytopenia in patients after cardiopulmonary bypass surgery: 616-092.12

Abstract

Summary. Introduction. If early postoperative thrombocytopenia is a result of dilution, the causes and mechanisms underlying late-onset thrombocytopenia are still poorly understood. We hypothesize that it results from endothelial damage, including complement-mediated one, leading to platelet-mediated thrombosis and reparative processes in the endothelium. Aim: to investigate the role of complement system activation and endothelial damage in the late-onset postoperative thrombocytopenia. Materials and Methods. Our prospective cohort observational study included 59 patients who underwent cardiac surgery with cardiopulmonary bypass. Platelet counts were measured 3 days after the intervention and a decrease below 100×109/L or sudden, more than 2-fold decrease were noted. We examined the emergence of endpoints (hypoxia, thrombosis, and death) depending on the concentrations of endothelial activation/damage markers, complement components, and natural anticoagulants. To determine the extent of endothelial activation or damage, we analyzed plasma levels of syndecan-1, heparan sulfate, E-selectin, P-selectin, RESAM-1, and VE-cadherin. We also evaluated the status of the endogenous anticoagulant system, including thrombomodulin, tissue factor pathway inhibitor, and antithrombin III. Additionally, we examined the activity of the complement system components C1q, C3a, C5a, membrane attack complex (MAC), mannose-binding lectin, and the complement system inhibitor factor H. Results. Thrombotic complications were found in 32.2% of cases (n = 19), and hypoxia was noted in 55.9% of cases (n = 33). The mortality rate was 36.6% (n=21). Factor H, MAC, and thrombomodulin levels were found to predict the lowest values of platelet count. Thrombomodulin levels were found to predict hypoxia (odds ratio (OR)=1.417; 95% confidence interval (CI)=1.097–1.832; p=0.008), MAC (OR=1.0; 95% CI=1.0–1.0; p=0.032) and C1q (OR=1.0; 95% CI=1.0–1.0; p=0.02). The concentration of syndecan-1 enabled prediction of thrombosis (OR = 0.943; 95% CI = 0.894–0.995; p = 0.032) as well as mortality (OR = 0.918; 95% CI = 0.865–0.975; p = 0.005). Conclusion. Late-onset postoperative thrombocytopenia suggests endothelial damage, which may occur in response to complement activation. Endothelial damage leads to hypoxia, thrombosis, and death of patients with late-onset postoperative thrombocytopenia.

For citation: Kupryashov A.A., Tokmakova K.A., Samuilova D.Sh., Svobodov A.A., Zhemarina I.B. Mechanisms of late-onset thrombocytopenia in patients after cardiopulmonary bypass surgery. Tromboz, gemostaz i reologiya. 2023;(4):49–58. (In Russ.).

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