The COVID-19 Arterial Thromboembolic Complications: From Inflammation to Immunothrombosis Through Antiphospholipid Autoantibodies

Roncati, Luca; Manenti, Antonio; Manco, Gianrocco; Farinetti, Alberto; Mattioli, Anna Vittoria

doi:10.1016/j.avsg.2020.12.006

Cited by 15 publications

(22 citation statements)

References 12 publications

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“…NK-MK in fact mean megakaryocytes cytoplasm has been consumed to produce neo-platelets, then released when still alive in the lung microcirculation with prothrombotic effects, which can be dramatically amplified by LAC. In accordance with the emerging evidence of aPL antibodies in COVID-19 [9], we here support a real LAC role in abnormal immunothrombosis and coagulopathy in a life-threatening subgroup of COVID-19 patients, advancing LAC test as potential prognostic risk marker under intensive care in COVID-19. In this setting, the simultaneous occurrence of venous and arterial thromboses, as reported in 3.7% of COVID-19 patients [10], should alert the clinicians towards a secondary aPL syndrome, whose catastrophic variant is precisely defined Asherson's syndrome from the rheumatologist Ronald Andrew Asherson [Dec 19, 1934, Cape Town (ZA)-May 06, 2008, Johannesburg (ZA)], who described the syndrome that bears his name in 1992 [11].…”

Section: Discussionsupporting

confidence: 90%

Abnormal immunothrombosis and lupus anticoagulant in a catastrophic COVID-19 recalling Asherson’s syndrome

Roncati

Corsi

Barbolini

2021

J Thromb Thrombolysis

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Background Coronavirus disease 2019 (COVID-19) is a complex disease with many clinicopathological aspects, including abnormal immunothrombosis, and the full comprehension of its pathogenetic mechanisms is urgently required. Methods/Results By means of a multidisciplinary approach, we here report a catastrophic COVID-19 in a 44-year-old Philippine male patient, discovered lupus anticoagulant (LAC)-positive shortly before death, occurred 8 days after hospitalization in a clinical scenario refractory to standard high acuity care recalling Asherson's syndrome (catastrophic antiphospholipid syndrome). Conclusion A parallelism between this severe form of COVID-19 and Asherson's syndrome can be so drawn. Both the diseases in fact exhibit hypercytokinemia, thrombotic microangiopathy, disseminated intravascular coagulation and multiple organ failure, they show a relationship with viral infections, and they are burdened by a high mortality rate. A genetic predisposition to develop these two overlapping conditions may be supposed. Keywords Coronavirus disease 2019 (COVID-19) • Abnormal immunothrombosis • Lupus anticoagulant (LAC) • Megakaryocytes • Antiphospholipid syndrome (Hughes syndrome) • Asherson's syndrome Highlights• COVID-19 is the most dramatic pandemic of the new millennium characterized by many clinicopathological facets, among which abnormal immunothrombosis • Abnormal immunothrombosis is a leading cause of COVID-19 related deaths, and its impact can be amplified by the presence of antiphospholipid autoantibodies, such as LAC • In this setting, the simultaneous occurrence of venous and arterial thromboses should alert the clinicians towards a secondary antiphospholipid syndrome, sometimes burdened by a catastrophic evolution in genetically predisposed patients • The catastrophic variant of a secondary antiphospholipid syndrome takes also the name of Asherson's syndrome, from the rheumatologist Ronald Andrew Asherson, who described it in 1992 • The implications of all this for future directions are in favor of a routine antiphospholipid testing in severe COVID-19 patients, and its introduction under intensive care as potential prognostic risk marker

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Section: Discussionsupporting

confidence: 90%

Abnormal immunothrombosis and lupus anticoagulant in a catastrophic COVID-19 recalling Asherson’s syndrome

Roncati

Corsi

Barbolini

2021

J Thromb Thrombolysis

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“…Type 3 hypersensitivity reaction of endothelial walls consisting of antigen-antibody complex-es with fibrinoid necrosis were observed with COVID-19 infection [37]. High antiphospholipid antibody levels are postulated as a pathway for hypercoagulation by enhancing platelet adhesion to fibrin and endothelium, and have been observed with COVID-19 infection [38][39][40]. ACE2 is the responsible receptor for the viral adhesion on endothelial cells and viral replication results in inflammatory cell infiltration, endothelial cell apoptosis, and microvascular prothrombotic effects [36].…”

Section: Discussionmentioning

confidence: 99%

A review of aortic thrombosis in COVID-19 infection

Karabulut

Kapici

Andronikashvili

et al. 2021

Exploration of Medicine

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Aim: As the novel coronavirus disease 2019 (COVID-19) pandemic impacts the global healthcare system, evolving data show increased frequency of arterial and venous thromboembolism among patients with COVID-19 infection. Aortic thrombus is a rare thrombotic event with a wide spectrum of clinical manifestations and potential catastrophic complications. This study aimed to elucidate the clinical manifestations, diagnosis and treatment dilemmas of aortic thrombus with COVID-19 infection and raise awareness among frontline medical providers. Aortic thrombosis is rare, but if not considered early in the course of COVID-19 infection, the data suggest that the diagnosis will probably not be made until potentially serious complications arise. Methods: Literature review was conducted between November 1, 2019, and November 14, 2020, on PubMed and Embase to identify publications regarding aortic thrombosis among COVID-19 cases. Results: Most of the patients were male with a median age of 67 years, and had comorbidities (most commonly hypertension, dyslipidemia and diabetes mellitus). In our study, underlying atherosclerosis, a common risk factor for aortic thrombus, was identified among 56% of the patients. Aortic thrombus was symptomatic in 62% of these patients and most commonly manifested itself as acute limb ischemia (46%), whereas 30% of cases were found incidentally during the investigation of elevated inflammatory markers or increased oxygen requirement. Treatment was individualized given the lack of established guidelines for aortic thrombus, including anticoagulation, systemic and catheter directed thrombolysis, and surgical thrombectomy. Overall mortality was found to be 30% in our study. Conclusions: Although rare, aortic thrombus has high morbidity and mortality, and can present without any symptoms or underlying aortic disease. Aortic thrombosis is rare, but if not considered early in the course of COVID-19 infection, the data suggest that the diagnosis will probably not be made until potentially serious complications arise.

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“…In medium and large arteries, this pathology involves the external VV as well, while the internal VV, because of their small caliber, thinner walls, and lower blood inflow, disappear as a direct result of the antecedent endothelial damage ( Fig , B ). 5 As shown, 6 the subsequent hypoxia in arterial walls produces hypoxia-inducible factor 1a, in turn releasing other substances, such as matrix metalloproteinases, macrophages, monocytes, and chemoattractant proteins, specific for secondary degenerative-inflammatory lesions. In addition to endothelin-1 and angiotensin II type 1, vasoconstrictors are active on the VV as well.…”

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confidence: 98%