Thrombotic events after AstraZeneca vaccine: What if it was related to dysfunctional immune response?

Billy, Eric; Clarot, F.; Depagne, Corinne; Korsia-Meffre, Stéphane; Rochoy, Michaël; Zorès, Florian

doi:10.1016/j.therap.2021.04.003

Cited by 12 publications

(20 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It should also be noted that similar mechanisms to those detailed above have been considered as a cause for the recently reported thrombotic events associated with COVID-19 adenovirus expressing spike protein vaccinations [130]. Specifically, capture of adenovirus by heparin sulphate chains could activate a compliment mediated cytokine storm, resulting in coagulation cascades [131]. Alternatively, S protein expressed by adenovirus-infected endothelial cells and subsequent interactions with ACE2 could downregulate ACE2 and increase the risk of thrombotic events [131].…”

Section: Thromboembolismmentioning

confidence: 81%

“…Specifically, capture of adenovirus by heparin sulphate chains could activate a compliment mediated cytokine storm, resulting in coagulation cascades [131]. Alternatively, S protein expressed by adenovirus-infected endothelial cells and subsequent interactions with ACE2 could downregulate ACE2 and increase the risk of thrombotic events [131]. However, the exact mechanisms of vaccine related thrombotic events are yet to be fully characterised.…”

Section: Thromboembolismmentioning

confidence: 99%

See 1 more Smart Citation

Role of the Renin–Angiotensin–Aldosterone and Kinin–Kallikrein Systems in the Cardiovascular Complications of COVID-19 and Long COVID

Cooper

Boyle

Jefferson

et al. 2021

IJMS

View full text Add to dashboard Cite

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is the virus responsible for the COVID-19 pandemic. Patients may present as asymptomatic or demonstrate mild to severe and life-threatening symptoms. Although COVID-19 has a respiratory focus, there are major cardiovascular complications (CVCs) associated with infection. The reported CVCs include myocarditis, heart failure, arrhythmias, thromboembolism and blood pressure abnormalities. These occur, in part, because of dysregulation of the Renin–Angiotensin–Aldosterone System (RAAS) and Kinin–Kallikrein System (KKS). A major route by which SARS-CoV-2 gains cellular entry is via the docking of the viral spike (S) protein to the membrane-bound angiotensin converting enzyme 2 (ACE2). The roles of ACE2 within the cardiovascular and immune systems are vital to ensure homeostasis. The key routes for the development of CVCs and the recently described long COVID have been hypothesised as the direct consequences of the viral S protein/ACE2 axis, downregulation of ACE2 and the resulting damage inflicted by the immune response. Here, we review the impact of COVID-19 on the cardiovascular system, the mechanisms by which dysregulation of the RAAS and KKS can occur following virus infection and the future implications for pharmacological therapies.

show abstract

Section: Thromboembolismmentioning

confidence: 81%

Section: Thromboembolismmentioning

confidence: 99%

Role of the Renin–Angiotensin–Aldosterone and Kinin–Kallikrein Systems in the Cardiovascular Complications of COVID-19 and Long COVID

Cooper

Boyle

Jefferson

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…Vaccines have the potential to interact with ACE-2, promoting its internalization and degradation, a phenomenon also observed in platelets, in which subunit 1 of protein S, but not subunit 2, binds to ACE-2, inducing a dose-dependent facilitation of aggregation and release of adenosine triphosphate [192]. The loss of ACE-2 receptor activity from the outer side of the cell membrane, mediated by the interaction between ACE-2 and spike proteins, results in less angiotensin inactivation, which increases thrombotic risk [189,194].…”

Section: Pathophysiological Hypothesesmentioning

confidence: 99%

“…The pathogenesis of hypercoagulability after vaccination remains poorly understood, and several questions are still open [186][187][188][189][190][191][192][193][194][195][196][197][198][199][200][201][202]. Both host and vaccine factors might be involved, with pathology, at least in part, being related to the vaccine-triggered autoimmune reaction [155].…”

Section: Pathophysiological Hypothesesmentioning

confidence: 99%

“…Although NET is useful and effective, numerous studies have shown its association with thrombosis [202]. The protein S, expressed by vaccines, also activates the complement system and can induce a cellular and humoral immune cascade against the virus favoring thrombosis [194]. Disproportionate inflammation can also increase endothelial adhesion and the release of TF, the true trigger of thrombin generation, a key enzyme in coagulation [187].…”

Section: Pathophysiological Hypothesesmentioning

confidence: 99%

See 1 more Smart Citation

COVID-19, Vaccines, and Thrombotic Events: A Narrative Review

Abrignani

Murrone

Luca

et al. 2022

JCM

View full text Add to dashboard Cite

The coronavirus disease 2019 (COVID-19), a deadly pandemic that has affected millions of people worldwide, is associated with cardiovascular complications, including venous and arterial thromboembolic events. Viral spike proteins, in fact, may promote the release of prothrombotic and inflammatory mediators. Vaccines, coding for the spike protein, are the primary means for preventing COVID-19. However, some unexpected thrombotic events at unusual sites, most frequently located in the cerebral venous sinus but also splanchnic, with associated thrombocytopenia, have emerged in subjects who received adenovirus-based vaccines, especially in fertile women. This clinical entity was soon recognized as a new syndrome, named vaccine-induced immune thrombotic thrombocytopenia, probably caused by cross-reacting anti-platelet factor-4 antibodies activating platelets. For this reason, the regulatory agencies of various countries restricted the use of adenovirus-based vaccines to some age groups. The prevailing opinion of most experts, however, is that the risk of developing COVID-19, including thrombotic complications, clearly outweighs this potential risk. This point-of-view aims at providing a narrative review of epidemiological issues, clinical data, and pathogenetic hypotheses of thrombosis linked to both COVID-19 and its vaccines, helping medical practitioners to offer up-to-date and evidence-based counseling to their often-alarmed patients with acute or chronic cardiovascular thrombotic events.

show abstract

Neurological manifestations with jugular vein thrombosis linked to an inflammatory profile may be a sequela of long COVID

Mendoza‐Portillo,

Aleman‐Navarro,

Prieto

et al. 2023

Neuroprotection

View full text Add to dashboard Cite

More than 670 million cases of coronavirus disease 2019 (COVID‐19) have been recorded worldwide in the 3 years since the start of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. About 45% of survivors of COVID‐19 develop a syndrome known as long‐term COVID, in which symptoms persist even months after the acute infection. About 76% of patients with long COVID experience neurological manifestations. Moreover, patients who have survived COVID‐19 have an increased risk of cerebral venous thrombosis. This case report describes a 41‐year‐old woman who developed neurological manifestations associated with jugular vein thrombosis 24 h after administration of the Oxford–AstraZeneca (ChAdOx1 nCoV‐19) vaccine (AstraZeneca‐Serum Institute of India). She had been infected with SARS‐CoV‐2 three months before vaccination. Although initially suspected to be a case of vaccine‐induced immune thrombotic thrombocytopenia (VITT) in view of her recent vaccination, the patient did not have any hallmarks of VITT, such as thrombocytopenia, an increased d‐dimer level, or antibodies against platelet factor‐4. Moreover, the neurological manifestations were associated with a high concentration of inflammatory cytokines, including interleukin (IL)‐6, IL‐17A, and IL‐21, and elevated neutrophil levels in cerebrospinal fluid, suggesting that inflammatory immune components had a role in the development of thrombotic events and pointing to an alternative diagnosis. In this case, the laboratory results indicated that the neurological manifestations associated with jugular vein thrombosis were not associated with VITT. Therefore, we propose that the thrombosis of the left jugular vein was a sequela of SARS‐CoV‐2 infection.

show abstract

Thrombotic events after AstraZeneca vaccine: What if it was related to dysfunctional immune response?

Cited by 12 publications

References 9 publications

Role of the Renin–Angiotensin–Aldosterone and Kinin–Kallikrein Systems in the Cardiovascular Complications of COVID-19 and Long COVID

Role of the Renin–Angiotensin–Aldosterone and Kinin–Kallikrein Systems in the Cardiovascular Complications of COVID-19 and Long COVID

COVID-19, Vaccines, and Thrombotic Events: A Narrative Review

Neurological manifestations with jugular vein thrombosis linked to an inflammatory profile may be a sequela of long COVID

Contact Info

Product

Resources

About