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1.
PLoS One ; 18(6): e0282939, 2023.
Article in English | MEDLINE | ID: covidwho-20233615

ABSTRACT

BACKGROUND: Blood coagulation abnormalities play a major role in COVID-19 pathophysiology. However, the specific details of hypercoagulation and anticoagulation treatment require investigation. The aim of this study was to investigate the status of the coagulation system by means of integral and local clotting assays in COVID-19 patients on admission to the hospital and in hospitalized COVID-19 patients receiving heparin thromboprophylaxis. METHODS: Thrombodynamics (TD), thromboelastography (TEG), and standard clotting assays were performed in 153 COVID-19 patients observed in a hospital setting. All patients receiving treatment, except extracorporeal membrane oxygenation (ECMO) patients (n = 108), were administered therapeutic doses of low molecular weight heparin (LMWH) depending on body weight. The ECMO patients (n = 15) were administered unfractionated heparin (UFH). RESULTS: On admission, the patients (n = 30) had extreme hypercoagulation by all integral assays: TD showed hypercoagulation in ~75% of patients, while TEG showed hypercoagulation in ~50% of patients. The patients receiving treatment showed a significant heparin response based on TD; 77% of measurements were in the hypocoagulation range, 15% were normal, and 8% remained in hypercoagulation. TEG showed less of a response to heparin: 24% of measurements were in the hypocoagulation range, 59% were normal and 17% remained in hypercoagulation. While hypocoagulation is likely due to heparin treatment, remaining in significant hypercoagulation may indicate insufficient anticoagulation for some patients, which is in agreement with our clinical findings. There were 3 study patients with registered thrombosis episodes, and all were outside the target range for TD parameters typical for effective thromboprophylaxis (1 patient was in weak hypocoagulation, atypical for the LMWH dose used, and 2 patients remained in the hypercoagulation range despite therapeutic LMWH doses). CONCLUSION: Patients with COVID-19 have severe hypercoagulation, which persists in some patients receiving anticoagulation treatment, while significant hypocoagulation is observed in others. The data suggest critical issues of hemostasis balance in these patients and indicate the potential importance of integral assays in its control.


Subject(s)
COVID-19 , Thrombophilia , Venous Thromboembolism , Humans , Heparin/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Anticoagulants/therapeutic use , Venous Thromboembolism/drug therapy , Hemostasis , Thrombophilia/drug therapy , Thrombophilia/etiology
2.
Arch Cardiol Mex ; 91(Suplemento COVID): 047-054, 2021 Dec 20.
Article in Spanish | MEDLINE | ID: covidwho-2315058

ABSTRACT

Coagulopathy and thrombosis associated with coronavirus disease 2019 (COVID-19) represent a major issue in the management of this disease. In the past months, clinical studies have demonstrated that COVID-19 patients present with a particular hypercoagulable state, in which a markedly increased D-dimer concomitant with increased levels of fibrinogen are observed. This hypercoagulable state leads to an increased risk of thrombosis, which seems to be higher among those patients with critical symptoms of COVID-19. The best therapeutic approach to prevent thrombotic events in COVID-19 has not been determined yet and several questions regarding thromboprophylaxis therapy, such as the time to initiate anticoagulation, type of anticoagulant and dose regimen, have emerged among physicians. To address these concerns, several medical societies have published position papers to provide the opinion of thrombosis experts on the management of coagulopathy and thrombosis associated with COVID-19. In line with this, the Latin America Cooperative Group of Hemostasis and Thrombosis (Grupo CLAHT) has constituted a panel of experts in thrombosis and hemostasis to discuss the available data on this topic. The aim of this review is to summarize the current evidence regarding hemostatic impairment and thrombotic risk in COVID-19 and to provide a carefully revised opinion of Latin American experts on the thromboprophylaxis and management of thrombotic events and coagulopathy in patients with suspected COVID-19.


La coagulopatía y la trombosis asociadas a la enfermedad por coronavirus 2019 (COVID-19) representan un problema importante en el manejo de esta enfermedad. Los estudios clínicos de los últimos meses han demostrado que los pacientes con COVID-19 presentan un estado de hipercoagulabilidad particular, en el que se observa un aumento notable del dímero D concomitante con niveles elevados de fibrinógeno. El estado de hipercoagulabilidad conduce a un mayor riesgo de trombosis, que parece ser mayor entre aquellos pacientes con síntomas críticos de COVID-19. El mejor enfoque terapéutico para prevenir los eventos trombóticos en esta nueva enfermedad aún no se ha determinado y han surgido varias preguntas con respecto a la tromboprofilaxia, como el momento adecuado para iniciar la anticoagulación, el tipo de anticoagulante y el régimen de dosis. Para abordar estas preocupaciones, varias sociedades médicas han publicado artículos de posición para brindar la opinión de expertos en trombosis sobre el manejo de la coagulopatía y trombosis asociadas a COVID-19. Grupo Cooperativo Latinoamericano de Hemostasia y Trombosis (Grupo CLAHT) ha convocado a un panel de expertos en trombosis y hemostasia para discutir los datos disponibles sobre este tema. El objetivo de esta revisión es resumir la evidencia actual con respecto al deterioro hemostático y el riesgo trombótico en el COVID-19 y proporcionar una opinión cuidadosamente revisada de los expertos latinoamericanos sobre la tromboprofilaxis y el manejo de eventos trombóticos y coagulopatía en pacientes con sospecha de COVID-19.


Subject(s)
Anticoagulants/therapeutic use , COVID-19 , Thrombosis , Venous Thromboembolism , COVID-19/complications , Consensus , Hemostasis , Humans , Latin America , Thrombosis/prevention & control , Thrombosis/therapy , Venous Thromboembolism/prevention & control , Venous Thromboembolism/therapy
3.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2289852
4.
Int J Mol Sci ; 23(23)2022 Nov 25.
Article in English | MEDLINE | ID: covidwho-2294928

ABSTRACT

Hemostasis reflects a homeostatic mechanism that aims to balance out pro-coagulant and anti-coagulant forces to maintain blood flow within the circulation. Simplistically, a relative excess of procoagulant forces can lead to thrombosis, and a relative excess of anticoagulant forces can lead to bleeding. There are a wide variety of congenital disorders associated with bleeding or thrombosis. In addition, there exist a vast array of autoimmune diseases that can also lead to either bleeding or thrombosis. For example, autoantibodies generated against clotting factors can lead to bleeding, of which acquired hemophilia A is the most common. As another example, autoimmune-mediated antibodies against phospholipids can generate a prothrombotic milieu in a condition known as antiphospholipid (antibody) syndrome (APS). Moreover, there exist various autoimmunity promoting environments that can lead to a variety of antibodies that affect hemostasis. Coronavirus disease 2019 (COVID-19) represents perhaps the contemporary example of such a state, with potential development of a kaleidoscope of such antibodies that primarily drive thrombosis, but may also lead to bleeding on rarer occasions. We provide here a narrative review to discuss the interaction between various autoimmune diseases and hemostasis.


Subject(s)
Antiphospholipid Syndrome , COVID-19 , Thrombosis , Humans , COVID-19/complications , Hemostasis , Thrombosis/complications , Anticoagulants , Autoantibodies , Hemorrhage/complications
5.
Wiad Lek ; 76(3): 634-639, 2023.
Article in English | MEDLINE | ID: covidwho-2303896

ABSTRACT

OBJECTIVE: The aim: To investigate the features of coagulation homeostasis in patients with liver cirrhosis (LC) in COVID-19 infection. PATIENTS AND METHODS: Materials and methods: At the clinical base of the Department of Propaedeutics of Internal Medicine, 32 patients with LC infected with COVID-19 were examined - 1 Group of patients. The study also included 30 patients with LC who were not infected with COVID-19 (2 Group of patients). RESULTS: Results: The analysis of the obtained data indicates disorders of the hemostasis system in patients with LC without the COVID-19 infection (Group 2), as well as in patients with LC at the time of being infected with COVID-19. The violation of the protein synthesis function of the liver is manifested through a decrease in the level of fibrinogen in blood serum (up to 2.0±0.5 gr/l in patients of Group 1 at the time of admission for inpatient care) and up to 21.9±0.5 gr/l in patients of group ІІ - р<0.05. This was accompanied by an acceleration of prothrombin time, thrombin time and activated partial thromboplastic time in patients with LC, as well as an increase in the level of antithrombin III. The level of D-dimer was reduced both in patients of group II and in patients of group I at the time of being infected with COVID-19. CONCLUSION: Conclusions: Changes in coagulation homeostasis characteristic of hypocoagulation syndrome have been established in patients with LC. COVID-19 infection in patients with LC leads to hypercoagulation, especially in patients with complicated stage of LC (ascites, encephalopathy, hepatorenal syndrome).


Subject(s)
Blood Coagulation Disorders , COVID-19 , Humans , COVID-19/complications , Blood Coagulation , Hemostasis , Blood Coagulation Disorders/complications , Liver Cirrhosis/complications
6.
Ann Hematol ; 102(6): 1307-1322, 2023 Jun.
Article in English | MEDLINE | ID: covidwho-2303196

ABSTRACT

The coagulation, fibrinolytic, anticoagulation, and complement systems are in delicate balance with the vessel wall endothelium ensuring appropriate hemostasis. Coagulopathy in coronavirus disease 2019 (COVID-19) is not a simple disorder of one hemostatic component but a complicated process affecting most of the hemostasis system. COVID-19 disturbs the balance between the procoagulant systems and the regulatory mechanisms. Here, we investigate the effect of COVID-19 on key hemostatic components, including platelets, endothelial cells, coagulation factors, fibrinolytic system, anticoagulant protein system, and complement system, to improve our understanding of the pathophysiological processes underlying COVID-19 coagulopathy based on evidence.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Hemostatics , Humans , Hemostatics/pharmacology , Endothelial Cells/metabolism , Hemostasis , Blood Coagulation Factors/metabolism , Blood Platelets/metabolism , Endothelium, Vascular/metabolism , Fibrinolysis
7.
Int J Mol Sci ; 24(7)2023 Mar 30.
Article in English | MEDLINE | ID: covidwho-2297409

ABSTRACT

The molecular mechanisms underlying cardiovascular complications after the SARS-CoV-2 infection remain unknown. The goal of our study was to analyze the features of blood coagulation, platelet aggregation, and plasma proteomics in COVID-19 convalescents with AMI. The study included 66 AMI patients and 58 healthy volunteers. The groups were divided according to the anti-N IgG levels (AMI post-COVID (n = 44), AMI control (n = 22), control post-COVID (n = 31), and control (n = 27)). All participants underwent rotational thromboelastometry, thrombodynamics, impedance aggregometry, and blood plasma proteomics analysis. Both AMI groups of patients demonstrated higher values of clot growth rates, thrombus size and density, as well as the elevated levels of components of the complement system, proteins modifying the state of endothelium, acute-phase and procoagulant proteins. In comparison with AMI control, AMI post-COVID patients demonstrated decreased levels of proteins connected to inflammation and hemostasis (lipopolysaccharide-binding protein, C4b-binding protein alpha-chain, plasma protease C1 inhibitor, fibrinogen beta-chain, vitamin K-dependent protein S), and altered correlations between inflammation and fibrinolysis. A new finding is that AMI post-COVID patients opposite the AMI control group, are characterized by a less noticeable growth of acute-phase proteins and hemostatic markers that could be explained by prolonged immune system alteration after COVID-19.


Subject(s)
COVID-19 , Myocardial Infarction , Humans , Proteomics , COVID-19/complications , SARS-CoV-2 , Myocardial Infarction/metabolism , Hemostasis , Inflammation , Plasma/metabolism
9.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2277416
10.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2276591
11.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2276455
12.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2256951
13.
Cardiovasc Res ; 119(8): 1624-1640, 2023 Jul 06.
Article in English | MEDLINE | ID: covidwho-2256197

ABSTRACT

The haemostatic system is pivotal to maintaining vascular integrity. Multiple components involved in blood coagulation have central functions in inflammation and immunity. A derailed haemostasis is common in prevalent pathologies such as sepsis, cardiovascular disorders, and lately, COVID-19. Physiological mechanisms limit the deleterious consequences of a hyperactivated haemostatic system through adaptive changes in gene expression. While this is mainly regulated at the level of transcription, co- and posttranscriptional mechanisms are increasingly perceived as central hubs governing multiple facets of the haemostatic system. This layer of regulation modulates the biogenesis of haemostatic components, for example in situations of increased turnover and demand. However, they can also be 'hijacked' in disease processes, thereby perpetuating and even causally entertaining associated pathologies. This review summarizes examples and emerging concepts that illustrate the importance of posttranscriptional mechanisms in haemostatic control and crosstalk with the immune system. It also discusses how such regulatory principles can be used to usher in new therapeutic concepts to combat global medical threats such as sepsis or cardiovascular disorders.


Subject(s)
COVID-19 , Cardiovascular Diseases , Hemostatics , MicroRNAs , Humans , COVID-19/genetics , Hemostasis/genetics , Gene Expression Regulation , Blood Coagulation/genetics , Cardiovascular Diseases/genetics , Cardiovascular Diseases/therapy , MicroRNAs/genetics
14.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2260660
15.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2260424
16.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2259134
17.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2258390
18.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2284506
19.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2282343
20.
Am J Hematol ; 98 Suppl 1: E1-E128, 2023 02.
Article in English | MEDLINE | ID: covidwho-2279721
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