Volume 28, Issue 131 (November & December 2020)                   J Adv Med Biomed Res 2020, 28(131): 296-303 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Moghimi M, Khodadadi K, Mortazavi Y. A Narrative Review on Evaluation of Hypercoagulability State in Severe Covid-19 Patients with Background Risk Factors. J Adv Med Biomed Res 2020; 28 (131) :296-303
URL: http://journal.zums.ac.ir/article-1-6084-en.html
1- Dept. of of Hematology-Medical Oncology, Vali-e-Asr Hospital, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran
2- Dept. of Internal Medicine, Vali-e-Asr Hospital, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran , khodadadikasra2020@gmail.com
3- Cancer Gene Therapy Research Center, Zanjan University of Medical Sciences, Zanjan, Iran
Abstract:   (143618 Views)

Coronavirus disease (COVID-19) can induce coagulopathy at the base of sepsis-induced coagulopathy (SIC), which is an important cause of death in these patients. Cytokine storm causes imbalance in coagulation and fibrinolytic system. A combination of hypercoagulability state, decrease or inhibition of fibrinolysis and endotheliopathy causes thromboembolic events. Underlying diseases such as diabetes and hypertension with a high rate of mortality in COVID-19 and some conditions like aging and obesity are the main disorders with hemostatic disturbance and increase of coagulopathy. Therefore, it seems that the combination of COVID-19 infection and these risk factors increase the risk of thromboembolic complications all together.

Full-Text [PDF 329 kb]   (155227 Downloads) |   |   Full-Text (HTML)  (2559 Views)  

✅ Underlying diseases such as diabetes and hypertension with a high rate of mortality in COVID-19 and some conditions like aging and obesity are the main disorders with hemostatic disturbance and increase of coagulopathy. Therefore, it seems that the combination of COVID-19 infection and these risk factors increase the risk of thromboembolic complications all together.


Type of Study: Review Article | Subject: Clinical medicine
Received: 2020/06/26 | Accepted: 2020/08/12 | Published: 2020/10/12

References
1. Huang C,WangY,LiX,et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China..Lancet.2020; 395(10223): 497-506. [DOI:10.1016/S0140-6736(20)30183-5]
2. Zhu N,YuD,Wang W, et al., A Novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med.2020. 382(8): 727-33. [DOI:10.1056/NEJMoa2001017]
3. Coronavirus Resource Center, https://coronavirus.jhu.edu/map.html ;2020[accessed 22 Sep 2020]
4. Kannan, S,shaikA,SheezaA,Hemalatha K. COVID-19 (Novel Coronavirus 2019)-recent trends. Eur Rev Med Pharmacol Sci. 2020. 24(4): 2006-2011.
5. Gibson P, Qin L, Puah S.COVID-19 acute respiratory distress syndrome (ARDS): clinical features and differences from typical pre-COVID-19 ARDS. Med J Aust. 2020;213(2):54-56.
6. Gandhi A, Görlinger K. Coagulopathy in COVID-19: Connecting the dots together. J Cardiac Crit Care TSS. 2020; 4(1): 47-50. [DOI:10.1055/s-0040-1712739]
7. Kitchens C. Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC). Hematology Am SocHematolEduc Program. 2009; 240-46. [DOI:10.1182/asheducation-2009.1.240]
8. IbaT,DiM,LevyJ,KitamuraN,Jecko T, et al. New criteria for sepsis-induced coagulopathy (SIC) following the revised sepsis definition: a retrospective analysis of a nationwide survey. BMJ Open. 2017;7(9):e017046. [DOI:10.1136/bmjopen-2017-017046]
9. 7(9).
10. Iba, TLevyJH,Wada H, et al. Differential diagnoses for sepsis‐induced disseminated intravascular coagulation: communication from the SSC of the ISTH. J ThrombHaemost . 2019;17(2):415-19. [DOI:10.1111/jth.14354]
11. IbaT,LevyJ,Thachil J, et al . The progression from coagulopathy to disseminated intravascular coagulation in representative underlying diseases. Thromb Res. 2019;179:11-14 [DOI:10.1016/j.thromres.2019.04.030]
12. IbaT,LevyJ,Yamakawa K, et al., Proposal of a two-step process for the diagnosis of sepsis-induced disseminated intravascular coagulation. 2019. 17(8): 1265. [DOI:10.1111/jth.14482]
13. Taylor F,TohC,Wada H, et al. Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. ThrombHaemost. 2001; 86(5): 1327-30. [DOI:10.1055/s-0037-1616068]
14. Connors J, Levy J. COVID-19 and its implications for thrombosis and anticoagulation.Blood. 2020. 135(23): 2033-40. [DOI:10.1182/blood.2020006000]
15. GuoW,LiM,DongY,et al. Diabetes is a risk factor for the progression and prognosis of COVID‐19. Diabetes Metab Res Rev. 2020 : e3319. 2020: p. e3319. [DOI:10.1002/dmrr.3319]
16. Ashton A Ware J. Thromboxane A2 receptor signaling inhibits vascular endothelial growth factor-induced endothelial cell differentiation and migration. Circ Res .2004. 95(4): 372-79. [DOI:10.1161/01.RES.0000138300.41642.15]
17. BikdeliB,MadhavanM,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 CollCardiol .2020. 75(23): 2950-73. [DOI:10.1016/j.jacc.2020.04.031]
18. VargaZ,FlammerA,Steiger P, et al., Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234): 1417-18. [DOI:10.1016/S0140-6736(20)30937-5]
19. Helms J,CharlesT,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: 1-10. [DOI:10.1007/s00134-020-06062-x]
20. Li P,BletA,Smyth D, et al. The science underlying COVID-19: implications for the cardiovascular system. Circulation. 2020; 142(1):68-78. [DOI:10.1161/CIRCULATIONAHA.120.047549]
21. TuW,CaoJ,YuL,HuX,Liu Q. Clinicolaboratory study of 25 fatal cases of COVID-19 in Wuhan. Int Care Med. 2020; 46:1117-20. [DOI:10.1007/s00134-020-06023-4]
22. Tang N,LiD,WangX,Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost.2020. 18(4): 844-47. [DOI:10.1111/jth.14768]
23. Zhang D,GuoR,Lei L, et al. COVID-19 infection induces readily detectable morphological and inflammation-related phenotypic changes in peripheral blood monocytes, the severity of which correlate with patient outcome. 2020. Preprint from medRxiv. [DOI:10.1101/2020.03.24.20042655]
24. PanigadaM,BottinoN,Tagliabue P, et al. Hypercoagulability of COVID‐19 patients in intensive care unit. A report of thromboelastography findings and other parameters of hemostasis. J ThrombHaemost . 2020;18(7):1738-42. [DOI:10.1111/jth.14850]
25. Chang J.C. Acute respiratory distress syndrome as an organ phenotype of vascular microthrombotic disease: based on hemostatic theory and endothelial molecular pathogenesis. ClinApplThrombHemost. 2019; 25: 1076029619887437. [DOI:10.1177/1076029619887437]
26. CiceriF,BerettaL,Scandroglio A, et al. Microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome (MicroCLOTS): an atypical acute respiratory distress syndrome working hypothesis. Crit Care Resusc. 2020;22(2):95-97
27. Skurk T, Lee YM, Hauner H. Angiotensin II and its metabolites stimulate PAI-1 protein release from human adipocytes in primary culture. Hypertension. 2001; 37(5): 1336-40. [DOI:10.1161/01.HYP.37.5.1336]
28. Takaya H,YoshijiH,Kawarantani H, et al. Decreased activity of plasma ADAMTS13 are related to enhanced cytokinemia and endotoxemia in patients with acute liver failure. Biomed Rep. 2017. 7(3): 277-85. [DOI:10.3892/br.2017.945]
29. KubaK,ImaiY,Rao S, et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nature Medicine .2005. 11(8): 875-79. [DOI:10.1038/nm1267]
30. Nicholls J, Peiris M. Good ACE, bad ACE do battle in lung injury, SARS. Nat Med. 2005. 11(8): 821-22. [DOI:10.1038/nm0805-821]
31. Zhou B,SheJ,WangY,Ma X. Utility of ferritin, procalcitonin, and C-reactive protein in severe patients with 2019 novel coronavirus disease. 2020. [DOI:10.21203/rs.3.rs-18079/v1]
32. Hoffmann M,Kleine-weber H,Schroeder S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. 2020. Cell . 2020;16;181(2):271-80 [DOI:10.1016/j.cell.2020.02.052]
33. SarduC,GambardellaJ,Bruno M, et al. Is COVID-19 an endothelial disease? Clinical and basic evidence. Clinical and Basic Evidence. Preprints. 2020, 2020040204 [DOI:10.20944/preprints202004.0204.v1]
34. GuanW. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med. 2020. 382(18): 1708-20.
35. Cui S,ChenS,Li X, et al. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J ThrombHaemost. 2020;18(6):1421-24. [DOI:10.1111/jth.14830]
36. Chen N. 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]
37. De Taeye B, Smith LH. Vaughan, Plasminogen activator inhibitor-1: a common denominator in obesity, diabetes and cardiovascular disease. CurrOpinPharmacol. 2005;5(2):149-54 [DOI:10.1016/j.coph.2005.01.007]
38. Johansson L. Tissue plasminogen activator, plasminogen activator inhibitor-1, and tissue plasminogen activator/plasminogen activator inhibitor-1 complex as risk factors for the development of a first stroke. 2000. 31(1): 26-32. [DOI:10.1161/01.STR.31.1.26]
39. Yao X, Li T,HeZ,et al. A pathological report of three COVID-19 cases by minimally invasive autopsies. 2020. 49: E009-E009. Zhonghua Bing Li XueZaZhi . 2020; 8;49(5):411-17
40. Boccia M,Aronnel L, Celia B, et al. COVID-19 and coagulative axis: review of emerging aspects in a novel disease.Int J Cardiopulmon Med Rehabil. 2020. 90(2). [DOI:10.4081/monaldi.2020.1300]
41. TianS,HuW,NiuL,et al. Pulmonary pathology of early phase 2019 novel coronavirus (COVID-19) pneumonia in two patients with lung cancer. J ThoracOncol. 2020;15(5):700-4 [DOI:10.1016/j.jtho.2020.02.010]
42. PrabhakaranP,WareL,White K, et al. Elevated levels of plasminogen activator inhibitor-1 in pulmonary edema fluid are associated with mortality in acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2003. 285(1): L20-8. [DOI:10.1152/ajplung.00312.2002]
43. Wang D, HuB, Hu C, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020. 323(11): 1061-9. [DOI:10.1001/jama.2020.1585]
44. Huang C. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020. 395(10223): 497-506. [DOI:10.1016/S0140-6736(20)30183-5]
45. Grant PJ. Diabetes mellitus as a prothrombotic condition. J Intern Med. 2007. 262(2): 157-72. [DOI:10.1111/j.1365-2796.2007.01824.x]
46. Carr ME. Diabetes mellitus: a hypercoagulable state. J DiabetComplicat. 2001; 15(1): 44-54. [DOI:10.1016/S1056-8727(00)00132-X]
47. Stein P,GoldmanJ,Matta F, et al. Diabetes mellitus and risk of venous thromboembolism. Am J Med Sci. 2009. 337(4): 259-64. [DOI:10.1097/MAJ.0b013e31818bbb8b]
48. PengY,LinY,ChenC,et al. Type 1 diabetes is associated with an increased risk of venous thromboembolism: A retrospective population-based cohort study. PLoS One. 2020. 15(1): e0226997. [DOI:10.1371/journal.pone.0226997]
49. ECAT ANGINA PECTORIS STUDY GROUP. Angina pectoris study: baseline associations of haemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography. Eur Heart J. 1993. 14(1): 8-17. [DOI:10.1093/eurheartj/14.1.8]
50. Stone MC, Thorp J. Plasma fibrinogen--a major coronary risk factor. J R Coll Gen Pract, 1985. 35(281): 565-9.
51. Li Y,ZhaoK,Wei H, et al. Dynamic relationship between D-dimer and COVID-19 severity. Br J Haematol. 2020. 190(1): e24-e27. [DOI:10.1111/bjh.16811]
52. Lip GY. Hypertension and the prothrombotic state. J Hum Hypertens, 2000. 14(10-11): 687-90. [DOI:10.1038/sj.jhh.1001051]
53. Pedrinelli R. Microalbuminuria and endothelial dysfunction in essential hypertension. Lancet, 1994. 344(8914): 8-14. [DOI:10.1016/S0140-6736(94)91047-2]
54. Blann AD. Von Willebrand factor and endothelial damage in essential hypertension. J Hum Hypertens. 1993; 7(2): 107-11.
55. Lip GY,BlannA,Jones A. Relation of endothelium, thrombogenesis, and hemorheology in systemic hypertension to ethnicity and left ventricular hypertrophy. Am J Cardiol. 1997. 80(12): 1566-71. [DOI:10.1016/S0002-9149(97)00749-2]
56. O Tabak, RGelisgen, H Uzun, et al. Hypertension and hemostatic/fibrinolytic balance disorders.ClinInvest Med. 2009.32(6):E285-92. [DOI:10.25011/cim.v32i6.10664]
57. Peng H,YehF, Simone G, et al. Relationship between plasma plasminogen activator inhibitor-1 and hypertension in American Indians: findings from the strong heart study. J Hypertens.2017. 35(9): 1787-93. [DOI:10.1097/HJH.0000000000001375]
58. Gavriilaki E. Increased thrombotic and impaired fibrinolytic response to acute exercise in patients with essential hypertension: the effect of treatment with an angiotensin II receptor blocker. J Hum Hypertens. 2014. 28(10): 606-9. [DOI:10.1038/jhh.2014.18]
59. Gleerup G, Vind J, Winther K. Platelet function and fibrinolytic activity during rest and exercise in borderline hypertensive patients. Eur J Clin Invest. 1995; 25(4): 266-70. [DOI:10.1111/j.1365-2362.1995.tb01558.x]
60. Kiechl S, Willeit J. The natural course of atherosclerosis. Part II: vascular remodeling. Bruneck Study Group. ArteriosclerThrombVasc Biol. 1999; 19(6): 1491-8. [DOI:10.1161/01.ATV.19.6.1491]
61. BalleisenL,BaileryJ,Epping P, et al. Epidemiological study on factor VII, factor VIII and fibrinogen in an industrial population: I. Baseline data on the relation to age, gender, body-weight, smoking, alcohol, pill-using, and menopause. ThrombHaemost. 1985. 54(2): 475-9. [DOI:10.1055/s-0038-1657877]
62. Loskutoff DJ, Sawdey M, Mimuro J. Type 1 plasminogen activator inhibitor. ProgHemostThromb. 1989; 9: 87-115.
63. Hashimoto Y,KobayashiA,Yamazaki N, et al. Relationship between age and plasma t-PA, PA-inhibitor, and PA activity. Thromb Res. 1987; 46(5): 625-33. [DOI:10.1016/0049-3848(87)90264-7]
64. Abbate R. Age-related changes in the hemostatic system. Int J Clin Lab Res. 1993;23(1): 1-3. [DOI:10.1007/BF02592271]
65. AbdolRazak NB. Cancer-associated thrombosis: An overview of mechanisms, risk factors, and treatment. Cancers (Basel). 2018; 10(10):380. [DOI:10.3390/cancers10100380]
66. Guan W,LiangW,Zhao Y, et al. Comorbidity and its impact on 1590 patients with COVID-19 in China: a nationwide analysis. EurRespir J. 2020. 55(5): 2000547. [DOI:10.1183/13993003.01227-2020]
67. Desai A. COVID-19 and cancer: lessons from a pooled meta-analysis. JCO Glob Oncol. 2020; 6: 557-59. [DOI:10.1200/GO.20.00097]
68. Merad M, Martin JC. Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages. Nat Rev Immunol. 2020. 20(6): 355-62. [DOI:10.1038/s41577-020-0331-4]
69. Joly BS, Siguret V, Veyradier A. Understanding pathophysiology of hemostasis disorders in critically ill patients with COVID-19. Intensive Care Med. 2020; 46(8): 1603-6. [DOI:10.1007/s00134-020-06088-1]

Send email to the article author


Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2025 CC BY-NC 4.0 | Journal of Advances in Medical and Biomedical Research

Designed & Developed by : Yektaweb