The stimulation of thrombosis by hypoxia

Gupta, Neha; Zhao, You Yang; Evans, Colin E.

doi:10.1016/j.thromres.2019.07.013

Cited by 360 publications

(333 citation statements)

References 72 publications

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“…The dysfunction of endothelial cells induced by infection results in excess thrombin generation and fibrinolysis shutdown, which indicated a hypercoagulable state in patient with infection, 12,13 such as COVID‐19. In addition, the hypoxia found in severe COVID‐19 can stimulate thrombosis through not only increasing blood viscosity, but also a hypoxia‐inducible transcription factor‐dependent signaling pathway 14 . As evidence, occlusion and microthrombosis formation in pulmonary small vessels of critical patient with COVID‐19 has been reported from a recent lung organ dissection 15 .…”

Section: Discussionmentioning

confidence: 93%

Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy

Tang

Bai

Chen

et al. 2020

Journal of Thrombosis and Haemostasis

3,274

107

3,385

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Background:A relatively high mortality of severe coronavirus disease 2019 is worrying, and the application of heparin in COVID-19 has been recommended by some expert consensus because of the risk of disseminated intravascular coagulation and venous thromboembolism. However, its efficacy remains to be validated. Methods:Coagulation results, medications, and outcomes of consecutive patients being classified as having severe COVID-19 in Tongji hospital were retrospectively analyzed. The 28-day mortality between heparin users and nonusers were compared, as was a different risk of coagulopathy, which was stratified by the sepsis-induced coagulopathy (SIC) score or D-dimer result.Results: There were 449 patients with severe COVID-19 enrolled into the study, 99 of them received heparin (mainly with low molecular weight heparin) for 7 days or longer. D-dimer, prothrombin time, and age were positively, and platelet count was negatively, correlated with 28-day mortality in multivariate analysis. No difference in 28-day mortality was found between heparin users and nonusers (30.3% vs 29.7%, P = .910). But the 28-day mortality of heparin users was lower than nonusers in patients with SIC score ≥4 (40.0% vs 64.2%, P = .029), or D-dimer >6-fold of upper limit of normal (32.8% vs 52.4%, P = .017). Conclusions:Anticoagulant therapy mainly with low molecular weight heparin appears to be associated with better prognosis in severe COVID-19 patients meeting SIC criteria or with markedly elevated D-dimer. K E Y W O R D Scoagulopathy, coronavirus disease 2019, D-dimer, low molecular weight heparin, sepsis

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Section: Discussionmentioning

confidence: 93%

Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy

Tang

Bai

Chen

et al. 2020

Journal of Thrombosis and Haemostasis

3,274

107

3,385

View full text Add to dashboard Cite

show abstract

“…The dysfunction of endothelial cells induced by infection results in excess thrombin generation and fibrinolysis shutdown, which indicated a hypercoagulable state in patient with infection [9,10]. In addition, hypoxia existed in severe pneumonia can stimulate thrombosis through not only increasing blood viscosity, but also a hypoxia-inducible transcription factor-dependent signaling pathway [11]. Hence, coagulopathy may be found in quite a lot patients with severe pneumonia.…”

Section: Resultsmentioning

confidence: 99%

Difference of coagulation features between severe pneumonia induced by SARS-CoV2 and non-SARS-CoV2

Yin

Huang

et al. 2020

J Thromb Thrombolysis

404

389

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Severe coronavirus disease 2019 is commonly complicated with coagulopathy, the difference of coagulation features between severe pneumonia induced by SARS-CoV2 and non-SARS-CoV2 has not been analyzed. Coagulation results and clinical features of consecutive patients with severe pneumonia induced by SARS-CoV2 (COVID group) and non-SARS-CoV2 (non-COVID group) in Tongji hospital were retrospectively analyzed and compared. Whether patients with elevated D-dimer could benefit from anticoagulant treatment was evaluated. There were 449 COVID patients and 104 non-COVID patients enrolled into the study. The 28-day mortality in COVID group was approximately twofold of mortality in non-COVID group (29.8% vs. 15.4%, P = 0.003), COVID group were older (65.1 ± 12.0 vs. 58.4 ± 18.0, years, P < 0.001) and with higher platelet count (215 ± 100 vs. 188 ± 98, ×10 9 /L, P = 0.015), comparing to non-COVID group. The 28-day mortality of heparin users were lower than nonusers In COVID group with D-dimer > 3.0 μg/mL (32.8% vs. 52.4%, P = 0.017). Patients with severe pneumonia induced by SARS-CoV2 had higher platelet count than those induced by non-SARS-CoV2, and only the former with markedly elevated D-dimer may benefit from anticoagulant treatment.

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“…HIFs are heterodimeric transcriptional factors consisting of HIFβ subunit, expressed by all nucleated cells, and HIF1α and HIF2α subunits (for HIF1 and HIF2, respectively). Hypoxia induces HIF2α subunits and decreases hydroxylation resulting in inducing or inhibition of many genes, including tissue factor (TF) and plasminogen-activator inhibitor-1 (PAI-1) [19,20]. We did not measure PAI-1 in our patients, but we could assume that it would be very high, as it is shed by endothelial cells like vWF.…”

Section: Discussionmentioning

confidence: 99%

High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study

et al. 2020

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Purpose: Little evidence of increased thrombotic risk is available in COVID-19 patients. Our purpose was to assess thrombotic risk in severe forms of SARS-CoV-2 infection. Methods:All patients referred to 4 intensive care units (ICUs) from two centers of a French tertiary hospital for acute respiratory distress syndrome (ARDS) due to COVID-19 between March 3rd and 31st 2020 were included. Medical history, symptoms, biological data and imaging were prospectively collected. Propensity score matching was performed to analyze the occurrence of thromboembolic events between non-COVID-19 ARDS and COVID-19 ARDS patients.Results: 150 COVID-19 patients were included (122 men, median age 63 [53; 71] years, SAPSII 49 [37; 64] points). Sixty-four clinically relevant thrombotic complications were diagnosed in 150 patients, mainly pulmonary embolisms (16.7%). 28/29 patients (96.6%) receiving continuous renal replacement therapy experienced circuit clotting. Three thrombotic occlusions (in 2 patients) of centrifugal pump occurred in 12 patients (8%) supported by ECMO. Most patients (> 95%) had elevated D-dimer and fibrinogen. No patient developed disseminated intravascular coagulation. Von Willebrand (vWF) activity, vWF antigen and FVIII were considerably increased, and 50/57 tested patients (87.7%) had positive lupus anticoagulant. Comparison with non-COVID-19 ARDS patients (n = 145) confirmed that COVID-19 ARDS patients (n = 77) developed significantly more thrombotic complications, mainly pulmonary embolisms (11.7 vs. 2.1%, p < 0.008). Coagulation parameters significantly differed between the two groups. Conclusion:Despite anticoagulation, a high number of patients with ARDS secondary to COVID-19 developed life-threatening thrombotic complications. Higher anticoagulation targets than in usual critically ill patients should therefore probably be suggested.

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The stimulation of thrombosis by hypoxia

Cited by 360 publications

References 72 publications

Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy

Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy

Difference of coagulation features between severe pneumonia induced by SARS-CoV2 and non-SARS-CoV2

High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study

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