Severe arterial thromboembolism in patients with Covid-19

Lameijer, Joost R. C.; Houte, Joris van; Berckel, Marijn Marthe Georgine van; Canta, Leo R.; Yo, Lonneke S.F.; Nijziel, Marten R.; Krietemeijer, G. Menno; Troquay, Stephanie; Buise, Marc P.; Hendriks, Joris

doi:10.1016/j.jcrc.2020.08.002

Cited by 5 publications

(3 citation statements)

References 18 publications

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“…thrombosis in severely ill patients. 1,8,9 This is not unusual, because reports of rare disease entities can appear seemingly contradictory, especially in the early phases of understanding a disease process. However, these observations also suggest that perhaps the underlying mechanism of COVID-19-associated arterial thrombosis is independent of the cytokine storm that occurs in patients with COVID-19-associated venous thrombosis.…”

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confidence: 99%

The mystery of COVID-19-associated arterial thrombosis

Shalhub

2021

Journal of Vascular Surgery

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I read with interest the article by Indes et al 1 regarding the arterial complications in patients with severe acute respiratory syndrome coronavirus (SARS-CoV)-2. Their study has added to the growing body of data on this unique viral complication. Coronavirus disease 2019 (COVID-19)-associated coagulopathy is associated with elevated fibrinogen, D-dimer, and C-reactive protein. Some centers have described higher-than-expected rates of venous thromboembolism. 2 Markedly elevated D-dimer levels have also been reported in association with severe COVID-19 infections and mortality. 2,3 The proposed hypotheses to explain the presence of venous thrombosis in COVID-19 have centered on a dysregulated inflammatory response manifesting as a cytokine storm, complement activation, and endothelial injury. 4,5 The observation of an increased risk of venous thrombosis in association with severe illness due to viral infections in itself is not novel. However, whether (and to what degree) severe COVID-19 infection is associated with a uniquely prothrombotic phenotype remains uncertain.Although venous thromboembolism has been reported in previous outbreaks of coronaviruses, including SARS-CoV-1 and Middle Eastern respiratory syndrome, and influenza A H1N1 acute respiratory distress syndrome, 6,7 the association between SARS-CoV-2 infection and arterial thrombosis has not been reported with other viral infections. The coagulopathy observed in patients with COVID-19 differs from the disseminated intravascular coagulopathy typically seen in sepsis. Specifically, the associated thrombocytopenia and prolonged activated partial thromboplastin time and/or prothrombin time have been mild. 4 This observation led to speculation that the arterial thrombosis is a direct result of SARS-CoV-2 infection of endothelial cells through the angiotensinconverting enzyme 2 receptor and subsequent endotheliitis. 5,8 Also intriguing is the unpredictable nature of this arterial thrombosis among patients infected with COVID-19. Indes et al, 1 and others, observed no correlation between COVID-19 disease severity and the degree of arterial thrombosis, although others have observed arterial

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confidence: 99%

The mystery of COVID-19-associated arterial thrombosis

Shalhub

2021

Journal of Vascular Surgery

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“…There was a statistically significant increase in acute ischemic stroke (1.5% vs. 0.2%) in patients with COVID-19 as compared to those with influenza, and this difference remained significant when adjusted for age, sex, and race ( 80 ). Multiple case series have demonstrated that ischemic stroke can be the presenting symptom of COVID-19 with high rate of mortality and residual morbidity, including paralysis and aphasia ( 81 ).…”

Section: Covid-19 Associated Coagulopathy Leads To Increased Venous and Arterial Thrombosismentioning

confidence: 99%

A Review of Pathophysiology, Clinical Features, and Management Options of COVID-19 Associated Coagulopathy

Goswami

MacArthur

Sridharan

et al. 2020

Shock

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There is increasing evidence that novel coronavirus disease 2019 (COVID-19) leads to a significant coagulopathy, a phenomenon termed “COVID-19 associated coagulopathy”. COVID-19 has been associated with increased rates of both venous and arterial thromboembolic events, a source of significant morbidity and mortality in this disease. Further evidence suggests a link between the inflammatory response and coagulopathy associated with COVID-19. This presents a unique set of challenges for diagnosis, prevention, and treatment of thrombotic complications. In this review, we summarize and discuss the current literature on laboratory coagulation disruptions associated with COVID-19 and the clinical effects of thromboembolic events including pulmonary embolism (PE), deep vein thrombosis (DVT), peripheral arterial thrombosis, and acute ischemic stroke in COVID-19. Endothelial injury and augmented innate immune response are implicated in the development of diffuse macro- and microvascular thrombosis in COVID-19. The pathophysiology of COVID-19 associated coagulopathy is an important determinant of appropriate treatment and monitoring of these complications. We highlight the importance of diagnosis and management of dysregulated coagulation in COVID-19 in order to improve outcomes in COVID-19 patients with thromboembolic complications.

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“…[ 1 – 5 ] Researchers speculated that SARS-CoV-2 infects endothelial cells through the angiotensin-converting enzyme 2 receptor leading to arterial thromboemboli. [ 6 , 7 ] However, reports describing the incidence of arterial thromboemboli vary, [ 2 , 7 , 8 ], and the mechanisms leading to occurrence of arterial thromboemboli in those patients remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Incidence and characteristics of arterial thromboemboli in patients with COVID-19

et al. 2021

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Background Studies have reported COVID-19 as an independent risk factor for arterial thromboemboli. Methods From a cross-sectional sample, we determined the incidence and location of arterial thromboemboli (myocardial infarction, ischemic stroke, peripheral artery), stratified by COVID-19 status, in the RECOVER database, which included data on patients at 45 United States medical centers in 22 states. Epidemiological factors, clinical characteristics and outcomes were collected through a combination of individual chart review and automatic electronic query and recorded in REDCap®. We investigated the association of baseline comorbidities on the development of arterial thromboemboli and analyzed results based on the presence or absence of concomitant COVID-19 infection, testing this association with Chi-squared. We also described use of anticoagulants and statins. Results Data were collected on 26,974 patients, of which 13,803 (51.17%) tested positive for COVID-19. Incidence of arterial thromboemboli during hospitalization was 0.13% in patients who tested positive for COVID-19 and 0.19% in patients who tested negative. Arterial thromboemboli tended to be more common in extremities than in core organs (heart, kidney, lung, liver) in patients with COVID-19, odds ratio 2.04 (95% CI 0.707 – 5.85). Patients with COVID-19 were less likely to develop an arterial thrombus when on baseline statin medication (p=0.014). Presence of metabolic syndrome predicted presence of core arterial thrombus (p=0.001) and extremity arterial thrombus (p=0.010) in those with COVID-19. Arterial thromboemboli were less common in patients with COVID-19 than in those who tested negative for COVID-19. Conclusions Presence of a composite metabolic syndrome profile may be associated with arterial clot formation in patients with COVID-19 infection.

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Severe arterial thromboembolism in patients with Covid-19

Cited by 5 publications

References 18 publications

The mystery of COVID-19-associated arterial thrombosis

The mystery of COVID-19-associated arterial thrombosis

A Review of Pathophysiology, Clinical Features, and Management Options of COVID-19 Associated Coagulopathy

Incidence and characteristics of arterial thromboemboli in patients with COVID-19

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