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.
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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.
Subject(s)
COVID-19 , Thrombosis , Humans , von Willebrand Factor , Hemostasis , Platelet Aggregation , Anticoagulants/pharmacologyABSTRACT
Background/Introduction: SARS-CoV-2 is notorious for its ability to cause damage to the respiratory system and myocardium, which can result in the development of acute respiratory distress syndrome and myocardial dysfunction. Purpose: The aim of our study was to assess the interaction between the severity of COVID-19 and echocardiographic parameters of myocardial dysfunction, as well as lung ultrasound data. Methods: 47 COVID-19 patients without signs of cardiovascular pathology were included in our study (33 in the moderate severity subgroup and 14 in the severe subgroup). All patients underwent comprehensive transthoracic echocardiography, including global longitudinal strain (GLS) of both ventricles, and lung ultrasound at days 1 and 9 of the disease. We used GLS cut-off values of 16% and 20% for LV and RV respectively. We performed the lung ultrasonography using an 8-zone protocol for each lung. The EACVI lung ultrasound scoring system for each region and ultrasound pattern was used. Results: At day 1, patients in the severe subgroup had a greater tricuspid gradient (22,0 [21,0;26,0] vs. 30,0 [24,0;34,5], p=0,04) and systolic pulmonary artery pressure (22,0 [21,0;26,0] vs. 30,0 [24,0;34,5], p=0,02). Moreover, we noted a decrease in the GLS RV index in COVID-19-patients in comparison with the generally accepted reference values (18,45 [15,8;21,0]). During the course of the disease, an increase in GLS RV was noted in both subgroups, which was especially pronounced among severe patients (18,5 [15,2;21,1] vs. 20,2 [15,8;22,0], p=0,038). Assessing the LV function, we noted a difference in the E/e (LV) ratio among severe and moderate subgroups (7,5 [6,8;9,34] vs. 9,5 [7,7;10,2], p=0,03). The GLS LV didn't differ between patient subgroups at day 1. We noted an increase in GLS LV at day 9 in both subgroups, but the difference reached significance among moderate patients (17,9 [15,8;20,1] vs. 19,5 [17,1;21,8], p=0,038). We observed a greater number of points assessing the B-lines among severe subgroup compared to moderate subgroup (19,5 [17,5;26,5] vs. 13,0 [7,0;18,0], p<0,01). Conclusion: Among COVID-19 patients without an underlying cardiovascular pathology the transient decrease in LV and RV function assessed via GLS was observed even among patients with moderate disease severity.
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Background/Introduction: There are numerous reports regarding the direct endothelial damage by the SARS-CoV-2 that can lead to activation of both plasma hemostasis and platelet aggregation. However, the mechanism of interaction between endothelium and haemostasis in COVID-19 remains unclear. Purpose: The aim of our study was to assess the relationship between each link of clot formation process (endothelial function, plasma coagulation, platelet aggregation) with the severity of the disease. Methods: 58 COVID-19 patients were included in our study. Patients were divided into moderate (n=39) and severe (n=18) subgroups. All patients underwent a flow-mediated dilation (FMD) test, impedance aggregation, rotational thromboelastometry, thrombodynamics and von Willebrand factor antigen (vWF: Ag) quantification. All measurements were repeated on days 3 (point 2) and 9 (point 3) of hospitalization. Results: COVID-19 patients demonstrated the enhanced plasma coagulation (clotting time, s 613,0 [480;820], clot growth rate, μm/min 32,75 [29,3;38,7]). At point 1 no significant difference in parameters of plasma coagulation between patients' subgroups was noted. At point 2 a significant decrease in the size (CS, μm 1278.0 [1216.5;1356.5] vs 965.0 [659.8;1098.0], p<0,01) and clot growth rate (μm/min 32,4 [29,2;35,0] vs 17,7 [10,3;24,4], p<0,01) under the influence of anticoagulants in the moderate subgroup compared with point 1 was observed. We didn't observe such phenomenon in severe subgroup. There was no significant difference in platelet aggregation between subgroups at point 1. During the course of the disease the patients in the moderate and severe subgroups demonstrated a significant increase in platelet aggregation induced by arachidonic acid and ADP (severe: AUC ARA 48,0 [25,0;59,0] vs 77,5 [55,8;92,7], p=0,04;AUC ADP 44,0 [41,0;56,0] vs 58,0 [45,5;69,0], p=0,04;moderate: AUC ARA 31,5 [19,8;50,7] vs 56,0 [39,0;76,0], p=0,01;AUC ADP 43,0 [20,0;59,0] vs 56,6 [50,3;70,5], p=0,04;), in moderate subgroup the significant increase in TRAP-induced aggregation was also noted (AUC TRAP 58,0 [41,0;69,5] vs 76,0 [58,3;81,5], p=0,048). There were no significant differences in the FMD-test results between the patient subgroups. FMD-test results were predominantly within the reference ranges (7,1 [4,0;8,8]). Patients in the severe subgroup had significantly higher levels of vWF: Ag (228,0 [205,3;240,7] vs 232,0 [226,0;423,0], p=0,03). Conclusion: SARS-CoV-2 infection was characterized by increased levels of vWF:Ag, that could represent the local endothelial damage, meanwhile there was no generalized endothelial dysfunction assessed via FMD-test in moderate to severe patients. At the same time the enhanced plasma coagulation in COVID-19 patients was observed.
ABSTRACT
Introduction: Coagulopathy plays a significant role in COVID-19 pathogenesis. Benefit from anticoagulation is well established in hospitalized patients. But since there is a lack of data on coagulopathy resolution: there is no consensus in guidelines if extended anticoagulation is required. Purpose: The purpose of our work was to analyze coagulation abnormalities at 2 to 5 months after moderate to severe COVID-19. Methods: COVID-19 reconvalescents (CR), discharged from our hospital, were called for follow-up at 2-3 (CR1 group, 21 patients) or 5-6 (CR2 group, 26 patients) months after discharge. All CR were not on the anticoagulation therapy by that time. In addition to clinical examination and standard lab tests, we performed an FMD-test to analyze endothelial function, impedance aggregometry to analyze platelet aggregation, and a thrombodynamics test to assess thrombogenesis and fibrinolysis. The control group was recruited before the pandemic started. Results: All CR were free from thrombotic complications after discharge from the hospital. Endothelial function was not significantly impaired in CR compared with control, and was still in the normal range (7,07, IQR (3,36;11,56) vs. 7,87 (5,42;13,45)). Platelet aggregation was significantly lower in CR1 than in the control group in ADP-induced mode (37, IQR (19;47) vs. 46, IQR (41;50), p=0,02) and didn't differ in other groups and other modes (Asa, TRAP-induced). Thrombodynamics tests revealed suppression of the clot formation process in both CR1 and CR2 compared with control. There were decreased clot growth rates (μm/min) (CR1/CR2: 27,1, IQR (26,1;29,2)/27,6, IQR (26,4;30,0) vs. 32,2, IQR (30,0;35,1), both p<0,001);decreased clot size (μm) (CR1/CR2: 1099, IQR (1069;1194)/1199, IQR (1058;1221) vs. 1304, IQR (1164;1380), both p<0,001), and decreased optical density (arb units) (CR1/CR2: 21'607, IQR (20'363;24'545)/22'741, IQR (21'344;25'961) vs. 26'556, IQR (24'672;29'387, p<0,001 and p=0,09 respectively. Fibrinolysis was enhanced in CR groups compared with control (lysis progression was significantly higher for CR2 only, CR1/CR2: 2,9, IQR (2,5;3,8)/3,8, IQR (2,6;5,4) vs. 2,5, IQR (1,1;3,4) %/min, p=0,087 and p=0,007 respectively;expected clot lysis time was shorter in both CR1 and CR2: 36,5, IQR (29,8;44,2)/31,7, IQR (24,3;42,7) vs. 65,9. IQR (36,3;95,5) min, p=0,019 and p=0,016 respectively). There was no statistical difference in clot formation and in fibrinolysis between CR1 and CR2. Conclusion: In the deferred period (2-5 months) of COVID-19 the fibrinolysis process remains still active whereas the process of clot formation is mostly suppressed. Endothelial function assessed via the FMD test is within the normal range in the post COVID period.