ABSTRACT
Objective. To assess the relationship between the severity of COVID-19 in patients without significant baseline cardiovascular pathology and various echocardiographic parameters of myocardial dysfunction. Material and methods. 46 patients with COVID-19 were included in our study: 33 patients of moderate severity and 13 - with severe disease. On days 1 and 9 upon admission, all patients underwent an echocardiographic study with standard assessment of the both ventricles function, as well as an assessment of their global longitudinal strain (GLS). Comparison of the studied parameters was carried out both between groups of patients and within each group in dynamics. Results. On day 1patients in the severe group had higher values of the systolic gradient on the tricuspid valve (22.0 [21.0;26.0] vs 30.0 [24.0;34.5] mm Hg, p = 0.02), systolic excursion of the plane of the tricuspid ring (2.3 [2.1;2.4] vs 2.0 [1.9;2.2] mm, p = 0.016), E/e' ratio (9.5 [7.7;8.9] vs 7.5 [6.8;9.3], p = 0.03). At day 9 among patients in the severe group, there was a decrease in end-diastolic (111.0 [100.0;120.0] vs 100.0 [89.0;105.0] ml, p = 0.03) and of end-systolic (35.5 [32.0;41, 2] vs 28.0 [25.0;31.8] ml, p < 0.01) volumes of the left ventricle. There was a decrease in GLS of the both ventricles compared to general accepted values. In dynamics, there was an increase in the GLS of the right ventricle in both groups, but it was more pronounced among severe group of patients (day 1 -18.5 [-15.2;-21.1] vs -20.2 [-15.8.1;-21.1] %, p = 0.03). The troponin levels were in the normal range. Conclusion. In COVID-19 patients without significant baseline cardiovascular pathology, there is a transient decrease in longitudinal strain of both ventricles, even in the absence of clinical and laboratory signs of acute myocardial injury.Copyright © Creative Cardiology 2021.
ABSTRACT
COVID-19 infection is characterized by different clinical presentations. The thrombotic complications play the leading role in COVID-19 infection. SARS-CoV-2 virus can activate hemostasis at different levels: pulmonary tissue damage with subsequent plasma coagulation activation;local endothelial dysfunction and platelet activation during the course of the disease. Routine use of the anticoagulation treatment seems reasonable in hospitalized patients with COVID-19.Copyright © Creative Cardiology 2021.
ABSTRACT
Objective: Hypercoagulation and high incidence of thrombosis during COVID-19 is well established. However, there is a lack of data, how it changes over time. The main purpose of our study was to access different parts of hemostasis in few months after acute disease. Material and methods. Patients discharged from our hospital were invited for follow up examination in 2,3-3,8 (group 1 - 55 pts) or 4,6-5,7 months (group 2 - 45 pts) after admission. Control group (37 healthy adults) had been collected before pandemic started. Standard coagulation tests, aggregometry, thrombodynamics and fibrinolysis results were compared between groups. Result(s): D-dimer was significantly higher, and was APPT was significantly lower in group 2 compared to group 1, while fibrinogen, prothrombin levels didn't differ. Platelet aggregation induced by ASA, ADP, TRAP, spontaneous aggregation didn't differ significantly between groups. Thrombodynamics revealed hypocoagulation in both group 1 and group 2 compared to control: V, mum/min 27,3 (Interquartile range (IQR) 26,3;29,4) and 28,3 (IQR 26,5;30,1) vs. 32,6 (IQR 30,4;35,9) respectively;all p < 0,001. Clot size and density in both group 1 and group 2 were significantly lower than in control group. Fibrinolysis appeared to be enhanced in x2 compared to control and group 1. Lysis progression, %/min was higher: 3,5 (2,5;4,8) vs. 2,4 (1,6;3,5) and 2,6 (2,2;3,4) respectively, all p < 0,05. Lysis onset time in both group 1 and group 2 was significantly shorter compared to control. Conclusion(s): We revealed normalization of parameters of clot formation process in 2-6 months after COVID-19, while fibrinolysis remained still enhanced. Further study is required to investigate the clinical significance of these changes.Copyright © Creative Cardiology 2021.
ABSTRACT
AIM: Analysis of the dynamics of different stages of clot formation and its lysis in patients with different COVID-19 severity. MATERIALS AND METHODS: We prospectively included 58 patients with COVID-19 (39 patients with moderate disease severity and 18 patients with severe disease) and 47 healthy volunteers as a control group. All participants underwent the assessment of flow-mediated dilation (FMD) of brachial artery, impedance aggregometry, rotational thromboelastometry and thrombodynamics. Von Willebrand factor antigen (vWF:Ag) quantification was also performed in patients with COVID-19. Measurements were repeated on the 3rd and 9th day of hospitalization. RESULTS: Compared to the control group, patients with COVID-19 showed reduced values of platelet aggregation and greater values of the clot growth rate, as well as its size and density. On the first day of hospitalization, we found no differences in the activity of plasma hemostasis and endogenous fibrinolysis between subgroups of patients. With the progression of the disease, the growth rate and size of the clot were higher in the severe subgroup, even despite higher doses of anticoagulants in this subgroup. An increase in platelet aggregation was noted during the progression of the disease, especially in the severe subgroup. There were no differences in the results of the FMD test by subgroups of patients. The vWF:Ag level was significantly higher in the severe subgroup. CONCLUSION: Thus, plasma hemostasis followed by secondary platelet activation correlates with the severity of COVID-19. Patients with moderate to severe coronavirus infection have predominantly local rather than generalized endothelial dysfunction.