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Особенности гемостаза у пациентов с коронавирусной инфекцией
Калинская А.И., Духин О.А., Молодцов И.А., Анисимова А.С., Сокорев Д.А., Елизарова А.К., Сапожникова О.А., Глебова К.А., Шахиджанов С.С., Спиридонов И.С., Атауллаханов Ф.И., Шпектор А.В., Васильева Е.Ю. Особенности гемостаза у пациентов с коронавирусной инфекцией. Терапевтический архив. 2022;94(7):876–883. DOI: 10.26442/00403660.2022.07.201754
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Kalinskaya AI, Dukhin OA, Molodtsov IA, Anisimova AS, Sokorev DA, Elizarova AK, Sapozhnikova OA, Glebova KA, Shakhidzhanov SS, Spiridonov IS, Ataullakhanov FI, Shpektor AV, Vasilieva EYu. Peculiarities of hemostasis in patients with COVID-19. Terapevticheskii Arkhiv (Ter. Arkh.). 2022;94(7):876–883.
DOI: 10.26442/00403660.2022.07.201754
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Аннотация
Цель. Анализ динамики разных этапов образования тромба и его лизиса у пациентов с различной тяжестью течения COVID-19.
Материалы и методы. Произведен анализ образцов 58 пациентов с COVID-19 (39 больных со средней тяжестью течения и 18 человек с тяжелым течением) и 47 здоровых добровольцев. Всем участникам проведены тест эндотелий-зависимой вазодилатации (ЭЗВД) плечевой артерии, импедансная агрегометрия, ротационная тромбоэластометрия и тест тромбодинамики. Пациентам с COVID-19 также выполнено измерение антигена фактора фон Виллебранда (ффВ:Аг). Измерения проводили в динамике на 3 и 9-й день госпитализации.
Результаты. По сравнению с контрольной группой у пациентов c COVID-19 выявлены сниженные значения агрегации тромбоцитов и большие значения скорости роста сгустка, а также его размера и плотности. В 1-й день госпитализации не обнаружено различий в активности плазменного гемостаза и эндогенного фибринолиза между подгруппами пациентов. С течением заболевания скорость роста и размер тромба оказались выше в подгруппе тяжелого течения, даже несмотря на более высокие дозы антикоагулянтов у этой подгруппы больных. Зафиксирован рост агрегации тромбоцитов в ходе заболевания, особенно в подгруппе тяжелого течения. Различий в результатах теста ЭЗВД между подгруппами пациентов не зарегистрировано. Уровень ффВ:Аг был статистически значимо выше в подгруппе тяжелого течения.
Заключение. Показано, что плазменный гемостаз с последующей вторичной активацией тромбоцитов коррелируют с тяжестью течения заболевания COVID-19. У пациентов со средним и тяжелым течением коронавирусной инфекции имеется преимущественно локальная, нежели генерализованная эндотелиальная дисфункция.
Ключевые слова: COVID-19, тромбоциты, плазменный гемостаз, эндотелий
Материалы и методы. Произведен анализ образцов 58 пациентов с COVID-19 (39 больных со средней тяжестью течения и 18 человек с тяжелым течением) и 47 здоровых добровольцев. Всем участникам проведены тест эндотелий-зависимой вазодилатации (ЭЗВД) плечевой артерии, импедансная агрегометрия, ротационная тромбоэластометрия и тест тромбодинамики. Пациентам с COVID-19 также выполнено измерение антигена фактора фон Виллебранда (ффВ:Аг). Измерения проводили в динамике на 3 и 9-й день госпитализации.
Результаты. По сравнению с контрольной группой у пациентов c COVID-19 выявлены сниженные значения агрегации тромбоцитов и большие значения скорости роста сгустка, а также его размера и плотности. В 1-й день госпитализации не обнаружено различий в активности плазменного гемостаза и эндогенного фибринолиза между подгруппами пациентов. С течением заболевания скорость роста и размер тромба оказались выше в подгруппе тяжелого течения, даже несмотря на более высокие дозы антикоагулянтов у этой подгруппы больных. Зафиксирован рост агрегации тромбоцитов в ходе заболевания, особенно в подгруппе тяжелого течения. Различий в результатах теста ЭЗВД между подгруппами пациентов не зарегистрировано. Уровень ффВ:Аг был статистически значимо выше в подгруппе тяжелого течения.
Заключение. Показано, что плазменный гемостаз с последующей вторичной активацией тромбоцитов коррелируют с тяжестью течения заболевания COVID-19. У пациентов со средним и тяжелым течением коронавирусной инфекции имеется преимущественно локальная, нежели генерализованная эндотелиальная дисфункция.
Ключевые слова: COVID-19, тромбоциты, плазменный гемостаз, эндотелий
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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.
Keywords: COVID-19, platelets, plasma hemostasis, endothelium
Полный текст
Список литературы
1. Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507-13. DOI:10.1016/S0140-6736(20)30211-7
2. Jenner WJ, Gorog DA. Incidence of thrombotic complications in COVID-19: On behalf of ICODE: The International COVID-19 Thrombosis Biomarkers Colloquium. J Thromb Thrombolysis. 2021;52(4):999-1006. DOI:10.1007/s11239-021-02475-7
3. Edler C, Schröder AS, Aepfelbacher M, et al. Dying with SARS-CoV-2 infection – an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med. 2020;134(4):1275-84. DOI:10.1007/s00414-020-02317-w
4. McGonagle D, Bridgewood C, Ramanan AV, et al. COVID-19 vasculitis and novel vasculitis mimics. Lancet Rheumatol. 2021;3(3):e224-33. DOI:10.1016/S2665-9913(20)30420-3
5. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
6. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8. DOI:10.1016/S0140-6736(20)30937-5
7. O’Sullivan JM, Gonagle DM, Ward SE, et al. Endothelial cells orchestrate COVID-19 coagulopathy. Lancet Haematol. 2020;7(8):e553‑5. DOI:10.1016/S2352-3026(20)30215-5
8. Manne BK, Denorme F, Middleton EA, et al. Platelet Gene Expression and Function in COVID-19 Patients. Blood. 2020;136(11):1317-29. DOI:10.1182/blood.2020007214
9. Bikdeli B, Madhavan MV, Jimenez D, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(23):2950-73. DOI:10.1016/j.jacc.2020.04.031
10. Thachil J, Tang N, Gando S, et al. ISTH interim guidance on recognition and management of coagulopathy in COVID-19. J Thromb Haemost. 2020;18(5):1023-6. DOI:10.1111/jth.14810
11. Калинская А.И., Саввинова П.П., Васильева Е.Ю., Шпектор А.В. Особенности тромбообразования и эндогенного фибринолиза у пациентов с острым коронарным синдромом. Российский кардиологический журнал. 2018;(9):12-6 [Kalinskaya AI, Savvinova PP, Vasilieva EYu, Shpektor AV. The specifics of clotting and endogenic fibrinolysis in acute coronary syndrome patients. Russian Journal of Cardiology. 2018;(9): 12-6 (in Russian)]. DOI:10.15829/1560-4071-2018-9-12-16
12. Dukhin OA, Kalinskaya A, Uzhakhova H, et al. Clot formation and endogenous fibrinolysis in acs patients compared to patients with a history of st elevation myocardial infarction. Atherosclerosis. 2020;315:e233. DOI:10.1016/j.atherosclerosis.2020.10.733
13. Rodriguez-Miguelez P, Seigler N, Harris RA. Ultrasound assessment of endothelial function: A technical guideline of the flow-mediated dilation test. J Vis Exp. 2016;(110):54011. DOI:10.3791/54011
14. Paniccia R, Priora R, Liotta AA, Abbate R. Platelet function tests: a comparative review. Vasc Health Risk Manag. 2015;11:133-48. DOI:10.2147/VHRM.S44469
15. Balandina AN, Serebriyskiy II, Poletaev AV, et al. Thrombodynamics – A new global hemostasis assay for heparin monitoring in patients under the anticoagulant treatment. PLoS One. 2018;13(6):e0199900. DOI:10.1371/journal.pone.0199900
16. Funderburg NT, Lederman MM. Coagulation and morbidity in treated HIV infection. Thromb Res. 2014;133Suppl. 1(01):S21-4. DOI:10.1016/j.thromres.2014.03.012
17. Yang J-R, Lo J, Ho Y-L, et al. Pandemic H1N1 and seasonal H3N2 influenza infection in the human population show different distributions of viral loads, which substantially affect the performance of rapid influenza tests. Virus Res. 2011;155(1):163-7. DOI:10.1016/j.virusres.2010.09.015
18. Wang CC, Chang CT, Lin CL, et al. Hepatitis C virus infection associated with an increased risk of deep vein thrombosis: A population-based cohort study. Medicine (Baltimore). 2015;94(38):e1585. DOI:10.1097/MD.0000000000001585
19. Geisbert TW, Young HA, Jahrling PB, et al. Pathogenesis of Ebola Hemorrhagic Fever in Primate Models: Evidence that Hemorrhage Is Not a Direct Effect of Virus-Induced Cytolysis of Endothelial Cells. Am J Pathol. 2003;163(6):2371-82. DOI:10.1016/S0002-9440(10)63592-4
20. Squizzato A, Gerdes VEA, Büller HR. Effects of human cytomegalovirus infection on the coagulation system. Thromb Haemost. 2005;93(3):403‑10. DOI:10.1160/TH04-08-0523
21. RECOVERY Collaborative Group. Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2021;397(10285):1637-45. DOI:10.1016/S0140-6736(21)00676-0
22. Panigada M, Bottino N, Tagliabue P, et al. Hypercoagulability of COVID-19 patients in intensive care unit: A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020;18(7):1738-42. DOI:10.1111/jth.14850
23. Carsana L, Sonzogni A, Nasr A, et al. Pulmonary post-mortem findings in a series of COVID-19 cases from northern Italy: a two-centre descriptive study. Lancet Infect Dis. 2020;20(10):1135-40. DOI:10.1016/S1473-3099(20)30434-5
24. Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46(6):1099-102. DOI:10.1007/s00134-020-06033-2
25. Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.
DOI:10.1038/s41577-020-0343-0. Erratum in: Nat Rev Immunol. 2020.
26. Goshua G, Pine AB, Meizlish ML, et al. Articles Endotheliopathy in COVID-19-associated coagulopathy : evidence from a single-centre, cross-sectional study. Lancet Haematol. 2020;7(8):e575-82. DOI:10.1016/S2352-3026(20)30216-7
27. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
28. Mancini I, Baronciani L, Artoni A, et al. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J Thromb Haemost. 2021;19(2):513-21. DOI:10.1111/jth.15191
29. Evans PC, Rainger GE, Mason JC, et al. Endothelial dysfunction in COVID-19: A position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. Cardiovasc Res. 2020;116(14):2177-84. DOI:10.1093/cvr/cvaa230
30. Ward SE, Curley GF, Lavin M, et al. Von Willebrand factor propeptide in severe coronavirus disease 2019 (COVID-19): evidence of acute and sustained endothelial cell activation. Br J Haematol. 2021;192(4):714-9. DOI:10.1111/bjh.17273
31. Shechter M, Shechter A, Koren-Morag N, et al. Usefulness of brachial artery flow-mediated dilation to predict long-term cardiovascular events in subjects without heart disease. Am J Cardiol. 2014;113(1):162‑7. DOI:10.1016/j.amjcard.2013.08.051
32. Vasilieva E, Vorobyeva I, Lebedeva A, et al. Brachial Artery Flow-mediated Dilation in Patients with Tako-Tsubo Cardiomyopathy. Am J Med. 2011;124(12):1176-9. DOI:10.1016/j.amjmed.2011.05.033
33. Maruhashi T, Kajikawa M, Kishimoto S, et al. Diagnostic Criteria of Flow-Mediated Vasodilation for Normal Endothelial Function and Nitroglycerin-Induced Vasodilation for Normal Vascular Smooth Muscle Function of the Brachial Artery. J Am Heart Assoc. 2020;9(2):e013915. DOI:10.1161/JAHA.119.013915
34. Pober JS, Sessa WC. Evolving functions of endothelial cells in inflammation. Nat Rev Immunol. 2007;7(10):803-15. DOI:10.1038/nri2171
35. Helms J, Tacquard C, Severac F, et al. High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med. 2020;46(6):1089-98. DOI:10.1007/s00134-020-06062-x
36. Ladikou EE, Sivaloganathan H, Milne KM, et al. Von Willebrand factor (vWF): Marker of endothelial damage and thrombotic risk in COVID-19? Clin Med (Lond). 2020;20(5):e178-82. DOI:10.7861/clinmed.2020-0346
37. Philippe A, Chocron R, Gendron N, et al. Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality. Angiogenesis. 2021;24(3):505-17. DOI:10.1007/s10456-020-09762-6
38. Hottz ED, Azevedo-Quintanilha IG, Palhinha L, et al. Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood. 2020;136(11):1330-41. DOI:10.1182/blood.2020007252
39. Abdi M, Hosseini Z, Shirjan F, et al. Effect of Aspirin on the prevention of pro-thrombotic states in hospitalized COVID-19 patients: Systematic review. Cardiovasc Hematol Agents Med Chem. 2022. DOI:10.2174/1871525720666220401102728
40. Zareef R, Diab M, Al Saleh T, et al. Aspirin in COVID-19: Pros and Cons. Front Pharmacol. 2022;13:849628. DOI:10.3389/fphar.2022.849628
41. RECOVERY Collaborative Group. Aspirin in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2022;399(10320):143-51. DOI:10.1016/S0140-6736(21)01825-0
42. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18(4):844-7. DOI:10.1111/jth.14768
43. Lippi G, Favaloro EJ. D-dimer is Associated with Severity of Coronavirus Disease 2019: A Pooled Analysis. Thromb Haemost. 2020;120(5):876-8. DOI:10.1055/s-0040-1709650
2. Jenner WJ, Gorog DA. Incidence of thrombotic complications in COVID-19: On behalf of ICODE: The International COVID-19 Thrombosis Biomarkers Colloquium. J Thromb Thrombolysis. 2021;52(4):999-1006. DOI:10.1007/s11239-021-02475-7
3. Edler C, Schröder AS, Aepfelbacher M, et al. Dying with SARS-CoV-2 infection – an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med. 2020;134(4):1275-84. DOI:10.1007/s00414-020-02317-w
4. McGonagle D, Bridgewood C, Ramanan AV, et al. COVID-19 vasculitis and novel vasculitis mimics. Lancet Rheumatol. 2021;3(3):e224-33. DOI:10.1016/S2665-9913(20)30420-3
5. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
6. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8. DOI:10.1016/S0140-6736(20)30937-5
7. O’Sullivan JM, Gonagle DM, Ward SE, et al. Endothelial cells orchestrate COVID-19 coagulopathy. Lancet Haematol. 2020;7(8):e553‑5. DOI:10.1016/S2352-3026(20)30215-5
8. Manne BK, Denorme F, Middleton EA, et al. Platelet Gene Expression and Function in COVID-19 Patients. Blood. 2020;136(11):1317-29. DOI:10.1182/blood.2020007214
9. Bikdeli B, Madhavan MV, Jimenez D, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(23):2950-73. DOI:10.1016/j.jacc.2020.04.031
10. Thachil J, Tang N, Gando S, et al. ISTH interim guidance on recognition and management of coagulopathy in COVID-19. J Thromb Haemost. 2020;18(5):1023-6. DOI:10.1111/jth.14810
11. Калинская А.И., Саввинова П.П., Васильева Е.Ю., Шпектор А.В. Особенности тромбообразования и эндогенного фибринолиза у пациентов с острым коронарным синдромом. Российский кардиологический журнал. 2018;(9):12-6 [Kalinskaya AI, Savvinova PP, Vasilieva EYu, Shpektor AV. The specifics of clotting and endogenic fibrinolysis in acute coronary syndrome patients. Russian Journal of Cardiology. 2018;(9): 12-6 (in Russian)]. DOI:10.15829/1560-4071-2018-9-12-16
12. Dukhin OA, Kalinskaya A, Uzhakhova H, et al. Clot formation and endogenous fibrinolysis in acs patients compared to patients with a history of st elevation myocardial infarction. Atherosclerosis. 2020;315:e233. DOI:10.1016/j.atherosclerosis.2020.10.733
13. Rodriguez-Miguelez P, Seigler N, Harris RA. Ultrasound assessment of endothelial function: A technical guideline of the flow-mediated dilation test. J Vis Exp. 2016;(110):54011. DOI:10.3791/54011
14. Paniccia R, Priora R, Liotta AA, Abbate R. Platelet function tests: a comparative review. Vasc Health Risk Manag. 2015;11:133-48. DOI:10.2147/VHRM.S44469
15. Balandina AN, Serebriyskiy II, Poletaev AV, et al. Thrombodynamics – A new global hemostasis assay for heparin monitoring in patients under the anticoagulant treatment. PLoS One. 2018;13(6):e0199900. DOI:10.1371/journal.pone.0199900
16. Funderburg NT, Lederman MM. Coagulation and morbidity in treated HIV infection. Thromb Res. 2014;133Suppl. 1(01):S21-4. DOI:10.1016/j.thromres.2014.03.012
17. Yang J-R, Lo J, Ho Y-L, et al. Pandemic H1N1 and seasonal H3N2 influenza infection in the human population show different distributions of viral loads, which substantially affect the performance of rapid influenza tests. Virus Res. 2011;155(1):163-7. DOI:10.1016/j.virusres.2010.09.015
18. Wang CC, Chang CT, Lin CL, et al. Hepatitis C virus infection associated with an increased risk of deep vein thrombosis: A population-based cohort study. Medicine (Baltimore). 2015;94(38):e1585. DOI:10.1097/MD.0000000000001585
19. Geisbert TW, Young HA, Jahrling PB, et al. Pathogenesis of Ebola Hemorrhagic Fever in Primate Models: Evidence that Hemorrhage Is Not a Direct Effect of Virus-Induced Cytolysis of Endothelial Cells. Am J Pathol. 2003;163(6):2371-82. DOI:10.1016/S0002-9440(10)63592-4
20. Squizzato A, Gerdes VEA, Büller HR. Effects of human cytomegalovirus infection on the coagulation system. Thromb Haemost. 2005;93(3):403‑10. DOI:10.1160/TH04-08-0523
21. RECOVERY Collaborative Group. Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2021;397(10285):1637-45. DOI:10.1016/S0140-6736(21)00676-0
22. Panigada M, Bottino N, Tagliabue P, et al. Hypercoagulability of COVID-19 patients in intensive care unit: A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020;18(7):1738-42. DOI:10.1111/jth.14850
23. Carsana L, Sonzogni A, Nasr A, et al. Pulmonary post-mortem findings in a series of COVID-19 cases from northern Italy: a two-centre descriptive study. Lancet Infect Dis. 2020;20(10):1135-40. DOI:10.1016/S1473-3099(20)30434-5
24. Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46(6):1099-102. DOI:10.1007/s00134-020-06033-2
25. Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.
DOI:10.1038/s41577-020-0343-0. Erratum in: Nat Rev Immunol. 2020.
26. Goshua G, Pine AB, Meizlish ML, et al. Articles Endotheliopathy in COVID-19-associated coagulopathy : evidence from a single-centre, cross-sectional study. Lancet Haematol. 2020;7(8):e575-82. DOI:10.1016/S2352-3026(20)30216-7
27. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
28. Mancini I, Baronciani L, Artoni A, et al. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J Thromb Haemost. 2021;19(2):513-21. DOI:10.1111/jth.15191
29. Evans PC, Rainger GE, Mason JC, et al. Endothelial dysfunction in COVID-19: A position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. Cardiovasc Res. 2020;116(14):2177-84. DOI:10.1093/cvr/cvaa230
30. Ward SE, Curley GF, Lavin M, et al. Von Willebrand factor propeptide in severe coronavirus disease 2019 (COVID-19): evidence of acute and sustained endothelial cell activation. Br J Haematol. 2021;192(4):714-9. DOI:10.1111/bjh.17273
31. Shechter M, Shechter A, Koren-Morag N, et al. Usefulness of brachial artery flow-mediated dilation to predict long-term cardiovascular events in subjects without heart disease. Am J Cardiol. 2014;113(1):162‑7. DOI:10.1016/j.amjcard.2013.08.051
32. Vasilieva E, Vorobyeva I, Lebedeva A, et al. Brachial Artery Flow-mediated Dilation in Patients with Tako-Tsubo Cardiomyopathy. Am J Med. 2011;124(12):1176-9. DOI:10.1016/j.amjmed.2011.05.033
33. Maruhashi T, Kajikawa M, Kishimoto S, et al. Diagnostic Criteria of Flow-Mediated Vasodilation for Normal Endothelial Function and Nitroglycerin-Induced Vasodilation for Normal Vascular Smooth Muscle Function of the Brachial Artery. J Am Heart Assoc. 2020;9(2):e013915. DOI:10.1161/JAHA.119.013915
34. Pober JS, Sessa WC. Evolving functions of endothelial cells in inflammation. Nat Rev Immunol. 2007;7(10):803-15. DOI:10.1038/nri2171
35. Helms J, Tacquard C, Severac F, et al. High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med. 2020;46(6):1089-98. DOI:10.1007/s00134-020-06062-x
36. Ladikou EE, Sivaloganathan H, Milne KM, et al. Von Willebrand factor (vWF): Marker of endothelial damage and thrombotic risk in COVID-19? Clin Med (Lond). 2020;20(5):e178-82. DOI:10.7861/clinmed.2020-0346
37. Philippe A, Chocron R, Gendron N, et al. Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality. Angiogenesis. 2021;24(3):505-17. DOI:10.1007/s10456-020-09762-6
38. Hottz ED, Azevedo-Quintanilha IG, Palhinha L, et al. Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood. 2020;136(11):1330-41. DOI:10.1182/blood.2020007252
39. Abdi M, Hosseini Z, Shirjan F, et al. Effect of Aspirin on the prevention of pro-thrombotic states in hospitalized COVID-19 patients: Systematic review. Cardiovasc Hematol Agents Med Chem. 2022. DOI:10.2174/1871525720666220401102728
40. Zareef R, Diab M, Al Saleh T, et al. Aspirin in COVID-19: Pros and Cons. Front Pharmacol. 2022;13:849628. DOI:10.3389/fphar.2022.849628
41. RECOVERY Collaborative Group. Aspirin in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2022;399(10320):143-51. DOI:10.1016/S0140-6736(21)01825-0
42. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18(4):844-7. DOI:10.1111/jth.14768
43. Lippi G, Favaloro EJ. D-dimer is Associated with Severity of Coronavirus Disease 2019: A Pooled Analysis. Thromb Haemost. 2020;120(5):876-8. DOI:10.1055/s-0040-1709650
________________________________________________
1. Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507-13. DOI:10.1016/S0140-6736(20)30211-7
2. Jenner WJ, Gorog DA. Incidence of thrombotic complications in COVID-19: On behalf of ICODE: The International COVID-19 Thrombosis Biomarkers Colloquium. J Thromb Thrombolysis. 2021;52(4):999-1006. DOI:10.1007/s11239-021-02475-7
3. Edler C, Schröder AS, Aepfelbacher M, et al. Dying with SARS-CoV-2 infection – an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med. 2020;134(4):1275-84. DOI:10.1007/s00414-020-02317-w
4. McGonagle D, Bridgewood C, Ramanan AV, et al. COVID-19 vasculitis and novel vasculitis mimics. Lancet Rheumatol. 2021;3(3):e224-33. DOI:10.1016/S2665-9913(20)30420-3
5. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
6. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8. DOI:10.1016/S0140-6736(20)30937-5
7. O’Sullivan JM, Gonagle DM, Ward SE, et al. Endothelial cells orchestrate COVID-19 coagulopathy. Lancet Haematol. 2020;7(8):e553‑5. DOI:10.1016/S2352-3026(20)30215-5
8. Manne BK, Denorme F, Middleton EA, et al. Platelet Gene Expression and Function in COVID-19 Patients. Blood. 2020;136(11):1317-29. DOI:10.1182/blood.2020007214
9. Bikdeli B, Madhavan MV, Jimenez D, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-Up: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(23):2950-73. DOI:10.1016/j.jacc.2020.04.031
10. Thachil J, Tang N, Gando S, et al. ISTH interim guidance on recognition and management of coagulopathy in COVID-19. J Thromb Haemost. 2020;18(5):1023-6. DOI:10.1111/jth.14810
11. Kalinskaya AI, Savvinova PP, Vasilieva EYu, Shpektor AV. The specifics of clotting and endogenic fibrinolysis in acute coronary syndrome patients. Russian Journal of Cardiology. 2018;(9): 12-6 (in Russian). DOI:10.15829/1560-4071-2018-9-12-16
12. Dukhin OA, Kalinskaya A, Uzhakhova H, et al. Clot formation and endogenous fibrinolysis in acs patients compared to patients with a history of st elevation myocardial infarction. Atherosclerosis. 2020;315:e233. DOI:10.1016/j.atherosclerosis.2020.10.733
13. Rodriguez-Miguelez P, Seigler N, Harris RA. Ultrasound assessment of endothelial function: A technical guideline of the flow-mediated dilation test. J Vis Exp. 2016;(110):54011. DOI:10.3791/54011
14. Paniccia R, Priora R, Liotta AA, Abbate R. Platelet function tests: a comparative review. Vasc Health Risk Manag. 2015;11:133-48. DOI:10.2147/VHRM.S44469
15. Balandina AN, Serebriyskiy II, Poletaev AV, et al. Thrombodynamics – A new global hemostasis assay for heparin monitoring in patients under the anticoagulant treatment. PLoS One. 2018;13(6):e0199900. DOI:10.1371/journal.pone.0199900
16. Funderburg NT, Lederman MM. Coagulation and morbidity in treated HIV infection. Thromb Res. 2014;133Suppl. 1(01):S21-4. DOI:10.1016/j.thromres.2014.03.012
17. Yang J-R, Lo J, Ho Y-L, et al. Pandemic H1N1 and seasonal H3N2 influenza infection in the human population show different distributions of viral loads, which substantially affect the performance of rapid influenza tests. Virus Res. 2011;155(1):163-7. DOI:10.1016/j.virusres.2010.09.015
18. Wang CC, Chang CT, Lin CL, et al. Hepatitis C virus infection associated with an increased risk of deep vein thrombosis: A population-based cohort study. Medicine (Baltimore). 2015;94(38):e1585. DOI:10.1097/MD.0000000000001585
19. Geisbert TW, Young HA, Jahrling PB, et al. Pathogenesis of Ebola Hemorrhagic Fever in Primate Models: Evidence that Hemorrhage Is Not a Direct Effect of Virus-Induced Cytolysis of Endothelial Cells. Am J Pathol. 2003;163(6):2371-82. DOI:10.1016/S0002-9440(10)63592-4
20. Squizzato A, Gerdes VEA, Büller HR. Effects of human cytomegalovirus infection on the coagulation system. Thromb Haemost. 2005;93(3):403‑10. DOI:10.1160/TH04-08-0523
21. RECOVERY Collaborative Group. Tocilizumab in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2021;397(10285):1637-45. DOI:10.1016/S0140-6736(21)00676-0
22. Panigada M, Bottino N, Tagliabue P, et al. Hypercoagulability of COVID-19 patients in intensive care unit: A report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020;18(7):1738-42. DOI:10.1111/jth.14850
23. Carsana L, Sonzogni A, Nasr A, et al. Pulmonary post-mortem findings in a series of COVID-19 cases from northern Italy: a two-centre descriptive study. Lancet Infect Dis. 2020;20(10):1135-40. DOI:10.1016/S1473-3099(20)30434-5
24. Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. 2020;46(6):1099-102. DOI:10.1007/s00134-020-06033-2
25. Teuwen LA, Geldhof V, Pasut A, Carmeliet P. COVID-19: the vasculature unleashed. Nat Rev Immunol. 2020;20(7):389-91.
DOI:10.1038/s41577-020-0343-0. Erratum in: Nat Rev Immunol. 2020.
26. Goshua G, Pine AB, Meizlish ML, et al. Articles Endotheliopathy in COVID-19-associated coagulopathy : evidence from a single-centre, cross-sectional study. Lancet Haematol. 2020;7(8):e575-82. DOI:10.1016/S2352-3026(20)30216-7
27. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. DOI:10.1056/NEJMoa2015432
28. Mancini I, Baronciani L, Artoni A, et al. The ADAMTS13-von Willebrand factor axis in COVID-19 patients. J Thromb Haemost. 2021;19(2):513-21. DOI:10.1111/jth.15191
29. Evans PC, Rainger GE, Mason JC, et al. Endothelial dysfunction in COVID-19: A position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. Cardiovasc Res. 2020;116(14):2177-84. DOI:10.1093/cvr/cvaa230
30. Ward SE, Curley GF, Lavin M, et al. Von Willebrand factor propeptide in severe coronavirus disease 2019 (COVID-19): evidence of acute and sustained endothelial cell activation. Br J Haematol. 2021;192(4):714-9. DOI:10.1111/bjh.17273
31. Shechter M, Shechter A, Koren-Morag N, et al. Usefulness of brachial artery flow-mediated dilation to predict long-term cardiovascular events in subjects without heart disease. Am J Cardiol. 2014;113(1):162‑7. DOI:10.1016/j.amjcard.2013.08.051
32. Vasilieva E, Vorobyeva I, Lebedeva A, et al. Brachial Artery Flow-mediated Dilation in Patients with Tako-Tsubo Cardiomyopathy. Am J Med. 2011;124(12):1176-9. DOI:10.1016/j.amjmed.2011.05.033
33. Maruhashi T, Kajikawa M, Kishimoto S, et al. Diagnostic Criteria of Flow-Mediated Vasodilation for Normal Endothelial Function and Nitroglycerin-Induced Vasodilation for Normal Vascular Smooth Muscle Function of the Brachial Artery. J Am Heart Assoc. 2020;9(2):e013915. DOI:10.1161/JAHA.119.013915
34. Pober JS, Sessa WC. Evolving functions of endothelial cells in inflammation. Nat Rev Immunol. 2007;7(10):803-15. DOI:10.1038/nri2171
35. Helms J, Tacquard C, Severac F, et al. High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med. 2020;46(6):1089-98. DOI:10.1007/s00134-020-06062-x
36. Ladikou EE, Sivaloganathan H, Milne KM, et al. Von Willebrand factor (vWF): Marker of endothelial damage and thrombotic risk in COVID-19? Clin Med (Lond). 2020;20(5):e178-82. DOI:10.7861/clinmed.2020-0346
37. Philippe A, Chocron R, Gendron N, et al. Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality. Angiogenesis. 2021;24(3):505-17. DOI:10.1007/s10456-020-09762-6
38. Hottz ED, Azevedo-Quintanilha IG, Palhinha L, et al. Platelet activation and platelet-monocyte aggregate formation trigger tissue factor expression in patients with severe COVID-19. Blood. 2020;136(11):1330-41. DOI:10.1182/blood.2020007252
39. Abdi M, Hosseini Z, Shirjan F, et al. Effect of Aspirin on the prevention of pro-thrombotic states in hospitalized COVID-19 patients: Systematic review. Cardiovasc Hematol Agents Med Chem. 2022. DOI:10.2174/1871525720666220401102728
40. Zareef R, Diab M, Al Saleh T, et al. Aspirin in COVID-19: Pros and Cons. Front Pharmacol. 2022;13:849628. DOI:10.3389/fphar.2022.849628
41. RECOVERY Collaborative Group. Aspirin in patients admitted to hospital with COVID-19 (RECOVERY): a randomised, controlled, open-label, platform trial. Lancet. 2022;399(10320):143-51. DOI:10.1016/S0140-6736(21)01825-0
42. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18(4):844-7. DOI:10.1111/jth.14768
43. Lippi G, Favaloro EJ. D-dimer is Associated with Severity of Coronavirus Disease 2019: A Pooled Analysis. Thromb Haemost. 2020;120(5):876-8. DOI:10.1055/s-0040-1709650
Авторы
А.И. Калинская*1,2, О.А. Духин1,2, И.А. Молодцов1, А.С. Анисимова2, Д.А. Сокорев1, А.К. Елизарова1,2, О.А. Сапожникова1, К.А. Глебова1, С.С. Шахиджанов3, И.С. Спиридонов3, Ф.И. Атауллаханов3,4, А.В. Шпектор2, Е.Ю. Васильева1,2
1 ГБУЗ «Городская клиническая больница им. И.В. Давыдовского» Департамента здравоохранения г. Москвы, Москва, Россия;
2 ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России, Москва, Россия;
3 ФГБУН «Центр теоретических проблем физико-химической фармакологии» РАН, Москва, Россия;
4 Пенсильванский университет, Филадельфия, США
*kalinskaya.anna@gmail.com
1 ГБУЗ «Городская клиническая больница им. И.В. Давыдовского» Департамента здравоохранения г. Москвы, Москва, Россия;
2 ФГБОУ ВО «Московский государственный медико-стоматологический университет им. А.И. Евдокимова» Минздрава России, Москва, Россия;
3 ФГБУН «Центр теоретических проблем физико-химической фармакологии» РАН, Москва, Россия;
4 Пенсильванский университет, Филадельфия, США
*kalinskaya.anna@gmail.com
________________________________________________
Anna I. Kalinskaya*1,2, Oleg A. Dukhin1,2, Ivan A. Molodtsov1, Aleksandra S. Anisimova2, Denis A. Sokorev1, Antonina K. Elizarova1,2, Olga A. Sapozhnikova1, Kseniya A. Glebova1, Soslan S. Shakhidzhanov3, Ilia S. Spiridonov3, Fazly I. Ataullakhanov3,4, Alexander V. Shpektor2, Elena Yu. Vasilieva1,2
1 Davydovsky City Clinical Hospital, Moscow, Russia;
2 Yevdokimov Moscow State University of Medicine and Dentistry, Moscow, Russia;
3 Center for Theoretical Problems of Physicochemical Pharmacology, Moscow, Russia;
4 University of Pennsylvania, Philadelphia, USA
*kalinskaya.anna@gmail.com
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