Serial Thromboelastography and the Development of Venous Thromboembolism in Critically Ill Patients With COVID-19

Marvi, Tanya; Stubblefield, William B; Tillman, Benjamin F.; Tenforde, Mark W; Patel, Manish; Lindsell, Christopher J.; Self, Wesley H.; Grijalva, Carlos G; Rice, Todd W.

doi:10.1097/cce.0000000000000618

Cited by 6 publications

(4 citation statements)

References 38 publications

(61 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…COVID-19 is also associated with thromboembolic disease, and increases the risk of venous and arterial thromboembolism events (Tomasoni et al 2020 ; Zhou et al 2020a ; Tang et al 2020 ; Ali and Spinler 2021 ; Danzi et al 2020 ; Wichmann et al 2020 ; Wichmann 2020 ; Gąsecka et al 2021 ; Kyriakoulis et al 2021 ; Heinrich et al 2022 ; Marvi et al 2022 ; Tsaplin et al 2021 ; Farkouh et al 2022 ; Epelbaum 2020 ; Takasu et al 2022 ; Hendren et al 2020 ). Both DIC and pulmonary embolism were very common in COVID-19 patients.…”

Section: Pathogenic Mechanisms Of Cardiovascular Damage In Covid-19mentioning

confidence: 99%

“…Platelet counts and fibrinogen levels were positively associated with maximum amplitude. The association between diminished maximum amplitude, platelet counts, fibrinogen and venous thromboembolism may suggest a relative consumptive coagulopathy in critical COVID-19 patients (Marvi et al 2022 ). Recently, the study by Tsaplin et al found that there was a significant correlation between the Caprini score and the risk of venous thromboembolism in COVID-19 patients.…”

Section: Pathogenic Mechanisms Of Cardiovascular Damage In Covid-19mentioning

confidence: 99%

See 1 more Smart Citation

Pathogenic mechanisms of cardiovascular damage in COVID-19

Shao,

Yin

2024

Mol Med

View full text Add to dashboard Cite

Background COVID-19 is a new infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Since the outbreak in December 2019, it has caused an unprecedented world pandemic, leading to a global human health crisis. Although SARS CoV-2 mainly affects the lungs, causing interstitial pneumonia and severe acute respiratory distress syndrome, a number of patients often have extensive clinical manifestations, such as gastrointestinal symptoms, cardiovascular damage and renal dysfunction. Purpose This review article discusses the pathogenic mechanisms of cardiovascular damage in COVID-19 patients and provides some useful suggestions for future clinical diagnosis, treatment and prevention. Methods An English-language literature search was conducted in PubMed and Web of Science databases up to 12th April, 2024 for the terms “COVID-19”, “SARS CoV-2”, “cardiovascular damage”, “myocardial injury”, “myocarditis”, “hypertension”, “arrhythmia”, “heart failure” and “coronary heart disease”, especially update articles in 2023 and 2024. Salient medical literatures regarding the cardiovascular damage of COVID-19 were selected, extracted and synthesized. Results The most common cardiovascular damage was myocarditis and pericarditis, hypertension, arrhythmia, myocardial injury and heart failure, coronary heart disease, stress cardiomyopathy, ischemic stroke, blood coagulation abnormalities, and dyslipidemia. Two important pathogenic mechanisms of the cardiovascular damage may be direct viral cytotoxicity as well as indirect hyperimmune responses of the body to SARS CoV-2 infection. Conclusions Cardiovascular damage in COVID-19 patients is common and portends a worse prognosis. Although the underlying pathophysiological mechanisms of cardiovascular damage related to COVID-19 are not completely clear, two important pathogenic mechanisms of cardiovascular damage may be the direct damage of the SARSCoV-2 infection and the indirect hyperimmune responses.

show abstract

Section: Pathogenic Mechanisms Of Cardiovascular Damage In Covid-19mentioning

confidence: 99%

Section: Pathogenic Mechanisms Of Cardiovascular Damage In Covid-19mentioning

confidence: 99%

Pathogenic mechanisms of cardiovascular damage in COVID-19

Shao,

Yin

2024

Mol Med

View full text Add to dashboard Cite

show abstract

“…Each 1 mm increase in baseline and peak MA was associated with a reduced risk of venous thromboembolism (reduced by 8% and 14%, respectively). Lower initial platelet counts and fibrinogen levels are also associated with an increased risk of venous thromboembolism, while platelet counts and fibrinogen levels are positively related to MA [ 75 ]. A consensus of the International COVID-19 Thrombosis Biomarkers Colloquium concluded that the viscoelastic test as a marker of coagulation and fibrinolysis may be useful in determining the prognosis of COVID-19-associated thrombosis.…”

Section: Diagnostic Markers Of Thrombosis In Covid-19 Patientsmentioning

confidence: 99%

Risk of Thrombosis during and after a SARS-CoV-2 Infection: Pathogenesis, Diagnostic Approach, and Management

Sutanto

Soegiarto

2023

Hematology Reports

View full text Add to dashboard Cite

Coronavirus disease 2019 (COVID-19) increases the risk of thromboembolic events, especially in patients with severe infections requiring intensive care and cardiorespiratory support. COVID-19 patients with thromboembolic complications have a higher risk of death, and if they survive, these complications are expected to negatively affect these patients’ quality of life. Moreover, recent data reported that the risk of thromboembolism remains high months after a COVID-19 infection. Therefore, understanding the pathogenesis of thrombosis in the setting of COVID-19 may facilitate the early prevention and treatment of COVID-19-associated thromboembolism to reduce concomitant morbidity, mortality, and disability. This review will first discuss the clinical characteristics of COVID-19 infections, particularly with regard to the underlying pathophysiology. Then, the pathogenesis of COVID-19-associated thrombosis at the molecular and cellular levels will be comprehensively reviewed. Next, the clinical manifestations of venous and arterial thromboembolism in COVID-19 as well as the potential benefits of several laboratory markers of thrombosis will be further discussed. Lastly, the preventive and therapeutic management of thromboembolism during and after COVID-19 will also be explained.

show abstract

“…The role played by serical and mucosal IgA responses, the total IgA generation rate from this response, and the involvement of its epitopes in COVID-19 severity and/or vaccination are largely poor explored areas [ 3 , 4 , 23 ] aside from notable instances such as frequent thromboembolisms in severe COVID-19 cases [ 24 , 25 , 26 , 27 ].…”

Section: Introductionmentioning

confidence: 99%

Mapping IgA Epitope and Cross-Reactivity between Severe Acute Respiratory Syndrome-Associated Coronavirus 2 and DENV

De-Simone,

Napoleão-Pêgo,

Lechuga

et al. 2023

Vaccines

View full text Add to dashboard Cite

Background: The newly introduced COVID-19 vaccines have reduced disease severity and hospitalizations. However, they do not significantly prevent infection or transmission. In the same context, measuring IgM and IgG antibody levels is important, but it does not provide information about the status of the mucosal immune response. This article describes a comprehensive mapping of IgA epitopes of the S protein, its cross-reactivity, and the development of an ELISA-peptide assay. Methods: IgA epitope mapping was conducted using SPOT synthesis and sera from RT-qPCR COVID-19-positive patients. Specific and cross-reacting epitopes were identified, and an evolutionary analysis from the early Wuhan strain to the Omicron variant was performed using bioinformatics tools and a microarray of peptides. The selected epitopes were chemically synthesized and evaluated using ELISA-IgA. Results: A total of 40 IgA epitopes were identified with 23 in S1 and 17 in the S2 subunit. Among these, at least 23 epitopes showed cross-reactivity with DENV and other organisms and 24 showed cross-reactivity with other associated coronaviruses. Three MAP4 polypeptides were validated by ELISA, demonstrating a sensitivity of 90–99.96% and a specificity of 100%. Among the six IgA-RBD epitopes, only the SC/18 epitope of the Omicron variants (BA.2 and BA.2.12.1) presented a single IgA epitope. Conclusions: This research unveiled the IgA epitome of the S protein and identified many epitopes that exhibit cross-reactivity with DENV and other coronaviruses. The S protein of variants from Wuhan to Omicron retains many conserved IgA epitopes except for one epitope (#SCov/18). The cross-reactivity with DENV suggests limitations in using the whole S protein or the S1/S2/RBD segment for IgA serological diagnostic tests for COVID-19. The expression of these identified specific epitopes as diagnostic biomarkers could facilitate monitoring mucosal immunity to COVID-19, potentially leading to more accurate diagnoses and alternative mucosal vaccines.

show abstract

Serial Thromboelastography and the Development of Venous Thromboembolism in Critically Ill Patients With COVID-19

Abstract: To test the hypothesis that relatively lower clot strength on thromboelastography maximum amplitude (MA) is associated with development of venous thromboembolism (VTE) in critically ill patients with COVID-19.

Cited by 6 publications

References 38 publications

Pathogenic mechanisms of cardiovascular damage in COVID-19

Pathogenic mechanisms of cardiovascular damage in COVID-19

Risk of Thrombosis during and after a SARS-CoV-2 Infection: Pathogenesis, Diagnostic Approach, and Management

Mapping IgA Epitope and Cross-Reactivity between Severe Acute Respiratory Syndrome-Associated Coronavirus 2 and DENV

Contact Info

Product

Resources

About