The hemostatic balance in patients with coronavirus disease 2019 (COVID-19) seems to be shifted toward a hypercoagulable state. The aim of the current study was to assess the associated coagulation alterations by point-of-care-diagnostics, focusing on details of clot formation and lysis in these severely affected patients.
The authors’ prospective monocentric observational study included critically ill patients diagnosed with COVID-19. Demographics and biochemical data were recorded. To assess the comprehensive hemostatic profile of this patient population, aggregometric (Multiplate) and viscoelastometric (CloPro) measures were performed in the intensive care unit of a university hospital at a single occasion. Coagulation analysis and assessment of coagulation factors were performed. Data were compared to healthy controls.
In total, 27 patients (21 male; mean age, 60 yr) were included. Impedance aggregometry displayed no greater platelet aggregability in COVID-19 in comparison with healthy controls (area under the receiver operating characteristics curve [AUC] in adenosine diphosphate test, 68 ± 37 U vs. 91 ± 29 U [Hodges–Lehmann 95% CI, −27 (−48 to −1); P = 0.043]; AUC in arachidonic acid test, 102 ± 54 U vs. 115 ± 26 U [Hodges–Lehmann 95% CI, −21 (−51 to 21); P = 0.374]; AUC in thrombin receptor activating peptide 6 test, 114 ± 61 U vs. 144 ± 31 U [Hodges–Lehmann 95% CI, −31 (−69 to −7); P = 0.113]). Comparing the thromboelastometric results of COVID-19 patients to healthy controls, the authors observed significant differences in maximum clot firmness in fibrin contribution to maximum clot firmness assay (37 ± 11 mm vs. 15 ± 4 mm [Hodges–Lehmann 95% CI, 21 (17 to 26); P < 0.001]) and lysis time in extrinsic activation and activation of fibrinolysis by tissue plasminogen activator assay (530 ± 327 s vs. 211 ± 80 s [Hodges–Lehmann 95% CI, 238 (160 to 326); P < 0.001]).
Thromboelastometry in COVID-19 patients revealed greater fibrinolysis resistance. The authors did not find a greater platelet aggregability based on impedance aggregometric tests. These findings may contribute to our understanding of the hypercoagulable state of critically ill patients with COVID-19.
Although critically ill patients with COVID-19 are at an increased risk for thromboembolic complications, the details of hemostatic balance regarding clot lysis and platelet contribution to clot formation are not well understood.
Despite increases in von Willebrand factor, platelet aggregability based on impedance aggregometry testing was not increased in critically ill COVID-19, although viscoelastometric testing noted fibrinolysis resistance. These findings contribute to our understanding of the hypercoagulable state of COVID-19 and may have important considerations for management strategies.