Activation Of Coagulation System Research Articles

Plućna tromboembolija i perikardni izliv kao kardiovaskularne komplikacije COVID-19 infekcije

Systemic activation of coagulation and pulmonary thrombo-inflammation with local vascular damage caused by SARS-CoV-2 infection increases the risk of developing thromboembolic complications: stroke, pulmonary arterial thrombosis (pulmonary thromboembolism) and deep vein thrombosis. Myopericarditis may occurs in COVID-19 patients as part of or after the onset of respiratory symptoms. Minor pericardial effusions up to 1 cm that accompany pericardial involvement are common. In our patient during hospitalization due to bilateral pneumonia caused by SARS-Cov-2 virus during a routine control of D-dimer, elevated values 2.3 fold higher than the reference range were observed, with elevated biomarkers of inflammation. She had symptoms of a respiratory infection and no pronounced clinical symptoms that would indicate pulmonary thromboembolism. MSCT pulmonary angiography was performed and low-risk thromboembolism was confirmed. Anticoagulant therapy was started - therapeutic doses of low molecular weight heparin (enoxaparin), which was extended after discharge from the hospital with DOAC (Rivaroxaban) according to the protocol for the treatment of pulmonary thromboembolism. At the control examination after 3 weeks, pericarditis with moderate pericardial effusion was determined. Anticoagulant therapy (DOAC) was extended with the inclusion of colchicine in the therapy according to the protocol for the treatment of pericarditis with effusion. After 3 months of hospitalization in our patient with mild respiratory symptoms, bronchopneumonia of the right lung developed with slightly elevated biomarkers of inflammation and normal values of D-dimer. With prescribed antibiotic therapy and current therapy (DOAC and colchicine), there was a withdrawal of symptoms and regression of pericardial effusion and a reduction in right ventricular overload. At the follow-up examination 5 months after hospitalization, complete regression of pericardial effusion was confirmed with normal biomarkers of inflammation and D-dimer values. It is advisable to exclude anticoagulant therapy (DOAC) with continued low-dose aspirin therapy.

Venous thromboembolism in non-critically ill patients with COVID-19 infection

BackgroundSystemic coagulation activation and thrombotic complications are frequent among critically ill patients with COVID-19. Limited data are available in non-intensive care unit (ICU) patients.PurposeTo determine the incidence, risk factors and prognosis of venous thromboembolism (VTE) in non-ICU COVID-19 patients.MethodsWe studied consecutive COVID-19 patients admitted to general ward at Strasbourg Hospital, France (25.02.2020–19.04.2020). The primary outcome was any VTE complication. The secondary outcome was the composite of death or transfer to ICU.ResultsAmong the 289 patients included (62.2 ± 17.0 years, 59.2% male), VTE occurred in 49 (17.0%). Padua prediction score for VTE was similar between VTE and non-VTE patients. VTE imaging tests were performed in 100 (34.6%) patients and VTE diagnosed in median 7 (3–11) days after admission. On-admission, time from symptom onset to admission (OR 1.07, CI 95% [1.00–1.16], P = 0.045), Improve score (OR 1.37, [1.02–1.83], P = 0.032), leukocyte count (OR 1.16, [1.06–1.27], P = 0.001) and lack of thromboprophylaxis (OR 27.85, CI 95% [9.35–82.95], P < 0.001) were independent predictors of VTE. The incidence of the composite of death or ICU transfer was 31.0% and more frequent among patients with VTE (47.9% vs. 27.9%, P = 0.01). Fever (OR 5.37, CI 95% [1.44–19.97], P = 0.012), VTE (OR 3.44, CI 95% [1.63–7.25], P = 0.001), lymphopenia (OR 0.32, 95% CI [0.15–0.71]; P = 0.005) and extent of COVID-19 evaluated by chest CT severity (OR 1.56, 95% CI [1.12–2.16]; P = 0.007) were independently associated with in-hospital death or transfer to ICU (Table 1, Fig. 1).ConclusionsThe 17.0% incidence of VTE in non-ICU patients with COVID-19 was associated with worse outcomes. Given the high incidence of VTE in ward patients, there is an urgent need to investigate the optimal anticoagulation regimen.

Karakteristike i lečenje koagulopatije udružene sa COVID-19

Coagulopathy in COVID-19 represents a thrombo-inflammatory condition, and it is one of the most important causes of morbidity and mortality in this disease. The occurrence of coagulopathy correlates with the intensity of the inflammatory response to SARS-Cov-2 virus infection, and its presence is characterized by laboratory markers of blood hypercoagulability and clinically pronounced prothrombotic condition. Although the mechanism of coagulopathy is not fully elucidated, dysregulated and overemphasized immune responses mediated by inflammatory cytokines, complement activation, leukocyte activation with release of free nucleic acids and histones into the circulation, hypoxia and endothelial damage play a very important role in its development. Thrombosis can occur in all parts of the circulatory system and is most often localized in the microcirculation and venous part of the vasculature. A number of studies have shown that the presence of thrombotic pulmonary embolism can be demonstrated by objective methods in approximately 15% of COVID-19 patients treated in intensive care units, while the incidence of total venous thromboembolism in this group of patients is over 20% despite antithrombotic prophylaxis. Although much less common than venous thrombosis, arterial thrombosis may also occur in COVID-19 patients, most often in the form of myocardial infarction, ischemic stroke and peripheral artery occlusion. Damage to the endothelium under the influence of virus or inflammatory response, activation of platelets and coagulation system with fibrin deposition leads to extensive thrombosis in the microcirculation of lungs and other tissues and directly contributes to respiratory failure, ARDS or multiorgan failure. Therefore, coagulopathy in COVID-19 is an integral part of the pathophysiological mechanism of the disease and contributes to its clinical manifestation and progression. Main laboratory characteristics of COVID-19 coagulopathy are elevated values of D-dimer in the blood, which occurs in the process of decomposition of precipitated fibrin under the action of fibrinolytic enzymes in the microcirculation of the lungs and other organs. Therefore, D-dimer values reflect the intensity of the inflammation in the lungs and have prognostic significance in recognizing patients at risk of serious complications and unfavorable course of the disease. In contrast to disseminated intravascular coagulation in sepsis, severe thrombocytopenia and hypofibrinogenemia as well as bleeding tendencies are rare in COVID-19 coagulopathy. Due to the high frequency and important role of coagulopathy in morbidity and mortality, the use of anticoagulant therapy is recommended in all hospitalized patients. However, the optimal way of treating coagulopathy and the intensity of antithrombotic prophylaxis are not known, and represent the subject of intensive research.

RELATIONSHIP BETWEEN PRE- AND POST-THROMBOSIS FACTORS IN PATIENTS WITH STAGE VD CKD TREATED BY LONG-TERM HEMODIALYSIS

The aim: To determine informative value of pre-thrombosis, post-thrombosis and anticoagulation factors as well as their correlations for assessment of hemostasis status in patients with stage VD CKD. Materials and methods: Potential predictors of thrombophilia development as well as their relationships depending on the level of molecular markers of hemostasis were studied in 88 patients with stage VD CKD undergoing long-term hemodialysis with the view to determine their informative value. Results: Accumulation of soluble fibrin (sF) was demonstrated to cause moderate reaction of D-dimer (D-d) being insufficient in the absence of reaction of anticoagulant component of hemostasis. Soluble fibrin levels were found to be associated with D-d concentration (r = 0.39) and functionally inactive prothrombin forms (FIPF) to some extent (r = -0.24). Accumulation of FIPF in individuals with high level of sF implies significant activation of blood coagulation system at the stage prior to thrombin formation. Absence of close relationship between pre- and post-thrombosis indices may be indicative of still preserved potential of anticoagulant component of hemostasis. Conclusions: Accumulation of FIPF is an early marker of activation of blood coagulation and possible thrombosis. Levels of sF correlate with pre-thrombosis (fibrinogen, FIPF) and post-thrombosis (D-d) factors being associated with inhibition of anticoagulation processes. Comprehensive study of basic components of hemostasis in patients with VD stage of chronic kidney disease offer broader opportunities in arranging prophylactic measures to prevent thrombophilia.

Sepsis and anticoagulant, is amputation a lifesaving surgery?

Patients with severe sepsis are associated with coagulation abnormalities ranging from minimal to major activation of coagulation system, which may lead to fulminant disseminated intravascular coagulation (DIC) and multiorgan failure. Lower extremity amputation is indicated to remove ischemic, infected, or necrotic tissue or locally unresectable tumor and, at times, may be lifesaving. Peripheral artery disease and diabetes are the leading causes of non-traumatic lower extremity amputation. Amputation of lower limb in patient of severe sepsis associated with coagulation abnormalities may be limb saving surgery but may not be lifesaving surgery as in our case patient died due to multiorgan failure.

РЕЗУЛЬТАТЫ МНОГОЦЕНТРОВОГО МОНИТОРИНГА ПОКАЗАТЕЛЕЙ ГЕМОСТАЗА У БОЛЬНЫХ COVID-19

Materials and methods: a prospective non-randomized pilot multicenter study of the informativeness and clinical significance of hemostasis laboratory tests in 1210 patients with COVID-19 in disease course, including favorable and unfavorable outcomes, was performed. Hemostasis was assessed using clotting tests and D-dimer concentration, thromboelastography (TEG) and thrombodynamics (TD). Results: comparison of COVID-19 laboratory parameters and clinical picture showed that 75% of patients have pronounced activation of the plasma coagulation system upon admission to the hospital. Hypercoagulation is recorded in all tests, reaching a maximum in patients with subtotal (CT-3) and total (CT-4) lung lesion and/or resuscitation patients with a clinical picture of pulmonary embolism and unfavorable outcome. Low molecular weight heparins (LMWH) in a standard dosage leads to suppression of the initial hypercoagulable syndrome in more than half of the patients (from 75 to 31%). All patients without LMWH laboratory effect developed thrombotic complications. For clotting tests, insufficient sensitivity to changes in hemostasis against the background of LMWH was revealed. The D-dimer test effectively correlates with the severity and outcomes of COVID-19, but is not suitable for the control of heparin therapy, which is associated with the effect of lysis of existing blood clots and the lack of response to a decrease in the coagulation activity of patients. Methods of thromboelastography and thrombodynamics effectively record a decrease in the activity of the coagulation system and can be used to control heparin therapy. The correlation coefficient between the methods was 0,77. The dynamic indices of D-dimers, TEG and TD in severe patients and, especially, in patients with fatal outcomes revealed the greatest sensitivity to the control of heparin therapy in the Thrombodynamics test, which allows, along with thrombosis, to record hypercoagulable states and the risk of bleeding, which are the outcome of thrombohemorrhagic syndrome in patients with COVID-19.

Fibrinolysis shut down in COVID-19 patients: Report on two severe cases with potential diagnostic and clinical relevance

•To date most reports on COVID-19 associated coagulopathy focused an increased activation of the plasmatic coagulation system.•Using a novel method to assess clot lysis we observed abnormalities in fibrinolysis in COVID-19 infection.•Our finding suggests that fibrinolysis system may contribute to the procoagulatory status in COVID-19 patients.

Progestin type affects the increase of heparanase level and procoagulant activity mediated by the estrogen receptor.

Does progestin have an effect on heparanase level and procoagulant activity? Progestin increases the heparanase level and procoagulant activity via the estrogen receptor and the magnitude of the effect depends on the progestin type. Users of combined oral contraceptives (COCs) containing third- and fourth-generation progestins have a higher risk of venous thrombosis compared to those employing second-generation progestins. Heparanase protein is capable of degrading heparan sulfate (HS) chains and enhancing activation of the coagulation system. We have previously demonstrated that estrogen enhances the expression and procoagulant activity of heparanase. Estrogen and progestin receptor positive breast carcinoma cell lines: EMT6, T47D and MCF-7 were compared to the MDA-231 breast carcinoma cell line devoid of these receptors. This observational study incorporated 45 users of third-generation COCs progestins, 21 users of fourth-generation COCs progestins and 28 individuals not using hormonal therapy and not pregnant per history. Second-generation progestin-levonorgestrel, third-generation progestin-desogastrel (DSG), an estrogen receptor antagonist-ICI 182.780 and a progestin receptor antagonist-mifepristone, were added to cell lines. Heparanase level and procoagulant activity, HS levels, tissue factor (TF) activity and factor Xa levels were evaluated in the plasma of the study group. Levonorgestrel and DSG increased heparanase levels in the cells and medium. The effect of DSG was more prominent and additive to that of estrogen. The effect was inhibited by ICI 182.780. In the plasma of COC users, heparanase procoagulant activity, HS levels, TF activity and factor Xa levels were significantly higher compared to controls. In COC pills containing the same dose of estrogen, the procoagulant effect of drospirenone was significantly stronger than that of DSG and gestodene. The limitations of the study include a small number of participants in each study group, although the results are statistically significant and evaluated by several different coagulation parameters. The study demonstrates a new mechanism through which progestin affects coagulation system activation and shows that this effect is progestin type-dependent. Development of a progestin derivative with an attenuated effect on heparanase procoagulant activity may reduce thrombotic risk. No external funding was sought for this study. Y.N. is named in a European patent application No. IL201200027 filed on 18 January 2012. Other authors have no conflict of interest to declare. N/A.

Coagulation markers as predictors for clinical events in COPD.

Activation of the blood coagulation system is a common observation in inflammatory diseases. The role of coagulation in COPD is underexplored. The study included 413 COPD patients and 49 controls from the 3-year Bergen COPD Cohort Study (BCCS). One hundred and forty-eight COPD patients were also examined during AECOPD. The plasma markers of coagulation activation, TAT complex, APC-PCI complex and D-dimer, were measured at baseline and during exacerbations by enzyme immunoassays. Differences in levels of the markers between stable COPD patients and controls, and between stable COPD and AECOPD were examined. The associations between coagulation markers and later AECOPD and mortality were examined by negative binomial and Cox regression analyses. TAT was significantly lower in stable COPD (1.03 ng/mL (0.76-1.44)) than in controls (1.28 (1.04-1.49), P = 0.002). During AECOPD, all markers were higher than in the stable state: TAT 2.56 versus 1.43 ng/mL, APC-PCI 489.3 versus 416.4 ng/mL and D-dimer 763.5 versus 479.7 ng/mL (P < 0.001 for all). Higher D-dimer in stable COPD predicted a higher mortality (HR: 1.60 (1.24-2.05), P < 0.001). Higher TAT was associated with both an increased risk of later exacerbations, with a yearly incidence rate ratio of 1.19 (1.04-1.37), and a faster time to the first exacerbation (HR: 1.25 (1.10-1.42), P = 0.001, all after adjustment). Activation of the coagulation system is increased during COPD exacerbations. Coagulation markers are potential predictors of later COPD exacerbations and mortality.

Activation of inflammatory/coagulation system following electrical cardioversion of patient with recent onset atrial fibrillation: an explorative study of the relation to white matter hyperintensities

Abstract Background White matter hyperintensities (WMH), assessed using Fazekas scale, are more prevalent in patients with atrial fibrillation (AF), although its pathophysiologic mechanism(s) is unclear. Purpose The study objective was to explore the association between cardiac, inflammatory and coagulation biomarkers and white matter hyperintensities in anticoagulant-naïve patients following electrical cardioversion (CV) of recent onset AF. Methods Patients with AF duration &amp;lt;48 hours were prospectively included. Brain magnetic resonance imaging (MRI), C-reactive protein (CRP), high-sensitivity troponin T (hs-TNT), NT-proBNP, Interleukin 6, P-selectin, D-dimer, prothrombin fragment 1+2, von Willebrand factor Ag, coagulation factor VIII C and fibrinogen, were obtained sequentially prior, after (2–4 hours) and 7–10 days following CV. Repeated measure analysis of variance was performed. Results Forty-three patients (84% males), aged 55±9.6 years, (mean±SD) with median CHA2DS2-VASc score 1 (interquartile range 0–1) were included. Sequential MRI showed no new brain lesions after CV, while WMH were present at baseline in 21/43 (49%) patients. Repeated measure analysis of variance revealed a statistically significant overall change for hs-TNT: F(2,84)=6.056, p=0.03, NT-proBNP: F(2,84)=106.02, p&amp;lt;0.001, P-selectin: F(2,84)=8.69, p&amp;lt;0.001 and vWF:Ag: F(2,84)=4.078, p=0.02. CRP, IL-6, coagulation factor VIII-C and fibrinogen showed the same pattern, however none reached statistical significance. Patients with WMH had persistent higher values for CRP, hs-TNT, D-dimer, prothrombin fragment 1+2 and fibrinogen prior and after CV, as values at 7–10 days coincided; however, statistical interaction was not significant. Conclusion Transient activation of inflammatory and coagulation systems during atrial fibrillation subsides within 7–10 days after electric cardioversion of recent onset atrial fibrillation. A tendency of higher degree of activation during atrial fibrillation was observed in patients with white matter hyperintensities. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Swedish Heart-Lung Foundation, Swedish Research Council, Correvio International Sárl (Geneva Switzerland), Selanders Stiftelse

Dynamics of innate immunity parameters in acute kidney injury after coronary artery bypass grafting

Acute kidney injury (AKI) developing after cardiac surgery remains unsolved issue despite the high level of surgical techniques as well as organ and tissue protection during artificial blood circulation. Various publications demonstrate that complications emerge in as many as 42% cases, whereas renal replacement therapy is required in up to 1-8% cases. Systemic inflammatory response syndrome and activation of the blood coagulation system largely underlie developing AKI finally resulting in acute renal failure. Release of large amounts of cytokines is associated with subclinical renal damage, primarily with blocking renal glomerular filtration. Measuring concentration of serum inflammatory markers that could reflect activity of inflammatory events is crucial for predicting and selecting treatment methods as well as for identifying predictors of severe course with opportunity of early onset renal replacement therapy after hospitalization. Objective of our study was to assess diagnostic and prognostic value of innate immunity parameters such as interleukin (IL) 6, 8, 10, 17, tumor necrosis factor alpha (TNFα), growth factor TGF-β1 in patients with acute kidney injury before and after CABG. Blood serum samples collected from 120 patients (males and females) with ischemic heart disease (IHD) were examined before and after CABG. It was found that patients with acute kidney injury had elevated serum level of cytokines IL-6, IL-8, IL-10, IL-17, TNFα, and TGF-β1 in all groups on day 1 and day 2 after surgery. Hence, we provided the data on more detailed investigation of immune alterations in cardiosurgical patients with AKI prepared for planned CABG.

Hemostasis in pregnant, parturient and puerperal women with preeclampsia

Introduction.Preeclampsia (PE) is a specific complication of pregnancy holding a lead place in maternal and perinatal morbidity and mortality worldwide. The development of PE in the maternal body is accompanied by severe hypercoagulation, disturbed anticoagulation and fibrinolytic systems. As a result, vascular microthrombosis in diverse organs with developing endothelial dysfunction, impaired utero-placental blood circulation emerge that leads to adverse perinatal outcomes.Aim:to study status of coagulation arm in pregnant women with moderate and severe PE, after delivery by cesarean section, to optimize management of the postoperative period.Materials and Methods.There were enrolled 50 pregnant women with PE: 16 with moderate and 34 with severe PE after surgical delivery. A status of coagulation arm was examined by evaluating major parameters in coagulogram (fibrinogen, activated partial thromboplastin time, prothrombin, international normalized ratio) as well as assay for early diagnostics of blood clotting disorders to reveal bleeding and thrombosis risks.Results.It was found that prior to surgery patients with severe PE had significantly increased clot growth rate (V) by 1.09-fold (p = 0.001), relative clot density (D) by 1.15-fold (p = 0.001), and time of spontaneous clot appearance (Tsp) was accelerated by 2-fold (p = 0.001) compared to moderate PE. After surgical delivery, patients from both groups had changes evidencing about activated coagulation system: increased V, D, as well as the Tsp. Upon that, all such parameters in patients with severe PE were significantly elevated: the V – by 1.25-fold (p = 0.005); the D – by 1.1-fold (p = 0.02); the Tsp was accelerated by 2-fold (p = 0.03) compared to patients with moderate PE. All parameters in both groups tended to normalize on day 5 after surgical delivery, but patients with severe PE were shown to have significantly increased the V – by 1.5-fold (p = 0.001); the D – by 1.14-fold (p = 0.001); the clot size – by 1.14-fold (p = 0.001); the Tsp – accelerated by 41 % (p = 0.001) compared to patients with moderate PE.Conclusion.Thus, patients with moderate and severe PE after surgical delivery by cesarean section were featured with markedly activated coagulation hemostasis, which may justify a prolonged use of low-molecular-weight heparins in the postoperative period, especially in patients with PE.

Combination of the therapy of the anticoagulants and Tivortin in patients with cardiac ishemia at COVID-19

Background. Аn L-arginine is a conditionally essential amino acid. The daily average requirement is 4.2 mg. The L-arginine exhibits angioprotective properties, regulates proliferation and apoptosis, oxidative processes, blocks platelet aggregation and has a fibrinolytic effect ‒ antithrombotic (prevents the adhesion of circulating platelets and leukocytes) for anti-inflammatory effects. The likelihood of developing thrombotic complications in all patients with COVID-19 is very high, such patients are recommended to double dosage of anticoagulants.&#x0D; Objective. To study the combination of the anticoagulant therapy and the drug Tivortin in patients with coronary artery disease with COVID-19.&#x0D; Materials and methods. 28 patients with the cardiac ischemia of the exertion stenocardia functional class II-III with COVID-19 were examined. The patients were divided into the main and control groups. One of the groups, in addition to the anticoagulant therapy Clexan 2 times 0.6 mg, have taken the drug Tivortin, manufactured by “Yuria-Pharm” (Ukraine), containing L-arginine (4.2 mg).&#x0D; Results. The therapy with the use of the nitrate oxide donors in combination with the anticoagulants in the main group showed an increase in exercise tolerance, in the SpO2 level, i.e., a decrease in hypoxia in the main group compared with the control group.&#x0D; Conclusions. The addition of Tivortin to the therapy of anticoagulants that inhibit the activity of the blood coagulation system may increase the chances of survival of patients hospitalized with COVID-19.

Stroke in a young adult with mild COVID-19 suggesting endotheliitis.

We present the case of a young adult with stroke and very mild coronavirus disease 2019 (COVID-19). Results of hematologic work-up suggest SARS-CoV-2-induced endotheliitis. No concurrent etiology for stroke was detected. This case illustrates the possibility of stroke in healthy SARS-CoV-2-infected patients without hyperinflammatory state or excessive systemic coagulation activation.

The Potential Role of Coagulation Factor Xa in the Pathophysiology of COVID-19: A Role for Anticoagulants as Multimodal Therapeutic Agents.

SARS-CoV-2 infection (COVID-19) results in local and systemic activation of inflammation and coagulation. In this review article, we will discuss the potential role of coagulation factor Xa (FXa) in the pathophysiology of COVID-19. FXa, a serine protease, has been shown to play a role in the cleavage of SARS-CoV-1 spike protein (SP), with the inhibition of FXa resulting in the inhibition of viral infectivity. FX is known to be primarily produced in the liver, but it is also expressed by multiple cells types, including alveolar epithelium, cardiac myocytes, and macrophages. Considering that patients with preexisting conditions, including cardiopulmonary disease, are at an increased risk of severe COVID-19, we discuss the potential role of increased levels of FX in these patients, resulting in a potential increased propensity to have a higher infectious rate and viral load, increased activation of coagulation and inflammation, and development of fibrosis. With these observations in mind, we postulate as to the potential therapeutic role of FXa inhibitors as a prophylactic and therapeutic treatment for high-risk patients with COVID-19.

Dabigatran, the oral anticoagulant of choice at discharge in patients with non-valvular atrial fibrillation and COVID-19 infection: the ANIBAL protocol.

Atrial fibrillation is a frequent complication among patients with severe coronavirus disease-2019 (COVID-19) infection. Both direct and indirect mechanisms through COVID-19 have been described to explain this relationship. COVID-19 infection increases the risk of developing both arterial and venous thrombotic complications through systemic coagulation activation, leading to increased mortality. Chronic oral anticoagulation is essential to reduce the thromboembolic risk among AF patients. Switching to low-molecular-weight heparin has been recommended during hospitalization for COVID-19 infection. Of note, at discharge, the prescription of direct oral anticoagulants may offer some advantages over vitamin K antagonists. However, oral anticoagulants should only be prescribed after the consideration of drug–drug interactions with antiviral therapies as well as of the risk of hepatotoxicity, which is common among individuals with severe COVID-19 pneumonia. Not all anticoagulants have the same risk of hepatotoxicity; dabigatran has shown a good efficacy and safety profile and could have a lower risk of hepatotoxicity. Furthermore, its metabolism by cytochrome P450 is absent and it has a specific reversal agent. Therefore, dabigatran may be considered as a first-line choice for oral anticoagulation at discharge after COVID-19 infection. In this review, the available information on the antithrombotic management of AF patients at discharge after COVID-19 infection is updated. In addition, a practical algorithm, considering renal and liver function, which facilitates the anticoagulation choice at discharge is presented.

MODERN PRINCIPLES OF MANAGEMENT OF WOMEN WITH ABNORMAL UTERINE BLEEDING, TAKING INTO ACCOUNT THE BLOOD COAGULATION SYSTEM STATE

Abnormal uterine bleeding in women of childbearing potential requires effective emergency care. To determine the features of disorders in the hemostasis system, 120 women were directly examined at the time of bleeding on admission to the hospital, during treatment on days 5−7 of the menstrual cycle, as well as after 6−12 months from the end of treatment. Determination of congenital and acquired defects of the hemostasis system became the main criterion for the selection of combined and isolated forms of abnormal uterine bleeding. Treatment measures for patients were etiopathogenetically selected and individually the intensity of bleeding, the degree of anemia, coagulation parameters were taken into account. The staged treatment involved stopping the bleeding, regulating the menstrual cycle and further preventing the bleeding. It has been found that uterine bleeding in reproductive age in the absence of etiopathogenetic treatment leads to the development of posthemorrhagic anemia. The severity and nature of bleeding is determined by the presence of defects in the platelet system of the hemostasis system with impaired platelet aggregation function. The study of total coagulation potential, primary hemostasis and the state of intravascular hemocoagulation in the patients using the methods for estimating the amount of platelet aggregation allows to detect and differentiate disorders in the hemostasis system. According to the results of the study, it can be concluded that the use of fibrinolysis inhibitors in the patients with abnormal uterine bleeding helps to increase the activity of the blood coagulation system and complete cessation of bleeding on the 2nd−5th day. Prophylactic administration of antifibrinolytic drugs from the first day of the menstrual cycle reduces blood loss, stabilizes menstrual function and significantly improves the psycho−emotional state of patients. Key words: abnormal uterine bleeding, blood clotting, fibrinolysis inhibitors.

COMPARISON OF PLASMA COAGULABILITY AFTER SHORT-TERM TREATMENT WITH ROSUVASTATIN VERSUS ATORVASTATIN IN UNSTABLE ANGINA PATIENTS

Statins are the integral medications for the management of patients with acute coronary syndrome including unstable angina (UA) with multiple pleiotropic effects. However, the influence of statins on the coagulation system is controversial. Our study aimed to explore the effects of atorvastatin and rosuvastatin in high doses on some coagulation parameters (prothrombin pool (PP) and soluble fibrin-monomer complexes (SFMC) concentration) after a 7-days follow-up period in patients with UA. We recruited 50 patients aged 55 to 70 years with progressive UA. Standard therapy according to ESC guidelines 2020 was recommended for all patients. Before treatment onset, they were divided into 2 groups: group A – 26 patients were prescribed atorvastatin, group R – 24 patients with rosuvastatin treatment. The blood samples to analyze the concentration of PP and SFMC were collected twice – before the treatment onset and 7 days after. We revealed significant decrease in PP concentration (p=0,02) and increase in SFMC concentration (p=0,01) in group A patients while there were no significant changes of investigated parameters (p=0,94, p=0,57 respectively) in group R. Additionally, we have noted significant negative correlation between baseline PP concentration and direction of PP changes (r=-0,803, p&lt;0,001) as well as PP changes direction and SFMC concentration after treatment (r=-0,655, p&lt;0,001). Thus, we may consider that atorvastatin and rosuvastatin are characterized by different influences on coagulation in patients with progressive UA with standard basic treatment. The rebound coagulation system activation after anticoagulant discontinuation is more pronounced in UA patients against a background of atorvastatin treatment in comparison with rosuvastatin.

Diagnosis, management, and outcomes of venous thromboembolism in COVID-19 positive patients: a role for direct anticoagulants?

Coronavirus disease 2019 (COVID-19) has been associated with an increased risk of thromboembolic complications due to systemic coagulation activation. Little is known about the role of direct anticoagulants (DOACs) in COVID-19 related thrombosis. In this audit we sought to distinguish COVID-19 hospitalised patients with a diagnosis of venous thromboembolism (VTE) and record their outcomes over a period of 3 months (01/02/2020–30/04/2020). A total of 1583 patients were diagnosed with laboratory proven COVID-19 disease. Amongst them, 38 patients (0.82%) suffered VTE (median age 68 years, male/female: 20/18). VTE was the presenting symptom on admission in 71%. Pulmonary embolism was diagnosed in 92% of patients; 5 patients required intensive care and 3 underwent thrombolysis. 27 patients received initial treatment with unfractionated heparin/low molecular weight heparin (LMWH) while 10 were treated with direct anticoagulants (DOACs). After a median follow up of 25 days, 29 (76%) patients were alive while 5 were still hospitalised. Most patients (83%) were discharged on DOACs, no VTE recurrence or bleeding was recorded post-discharge. Our results suggest that direct anticoagulants could be a safe and effective treatment option in selected COVID-19 positive patients who have suffered venous thromboembolism.

Cultivating a Better Understanding of COVID-19 Amidst a Shifting Landscape.

As COVID-19 swept across the globe, emergency physicians stood on the front lines of a pandemic unlike any seen in our lifetimes. In areas where cases surged, we rapidly assessed and stabilized large numbers of critically ill patients using the limited data available to us, for that is, fundamentally, what we do. In the beginning, we relied on first principles. Vital signs are vital. Isolate the infected. Intubate ARDS early.