The coagulopathy, endotheliopathy, and vasculitis of COVID-19

Abstract

Background COVID-19-associated coagulopathy (CAC) characterized by the elevated D-dimer without remarkable changes of other global coagulation markers is associated with various thrombotic complications and disease severity. The purpose of this review is to elucidate the pathophysiology of this unique coagulopathy. Methods The authors performed online search of published medical literature through PubMed using the MeSH (Medical Subject Headings) term "COVID-19," "SARS-CoV-2," "coronavirus," "coagulopathy," and "thrombus." Then, selected 51 articles that closely relevant to coagulopathy in COVID-19. Results The primary targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the pneumocytes, immune cells, and vascular endothelial cells. The alveolar damage and the pulmonary microvascular thrombosis are the major causes of acute lung injury in COVID-19. The endotheliopathy that occurs is due to direct SARS-CoV-2 infection and activation of other pathways that include the immune system and thromboinflammatory responses leading to what is termed CAC. As a result, both microvascular and macrovascular thrombotic events occur in arterial, capillary, venule, and large vein vascular beds to produce multiorgan dysfunction and thrombotic complications. In addition to the endothelial damage, SARS-CoV-2 also can cause vasculitis and presents as a systemic inflammatory vascular disease. Clinical management of COVID-19 includes anticoagulation but novel therapies for endotheliopathy, hypercoagulability, and vasculitis are needed. Conclusion The endotheliopathy due to direct endothelial infection with SARS-COV-2 and the indirect damage caused by inflammation play the predominant role in the development of CAC. The intensive control of thromboinflammation is necessary to improve the outcome of this highly detrimental contagious disease.

Neuroimaging manifestations in children with SARS-CoV-2 infection: a multinational, multicentre collaborative study

“… 31 It is also reported that thrombotic microangiopathy related to direct or indirect damage by SARS-CoV-2 to the vascular endothelium can occur. 32 In our case, the punctate signal abnormalities largely resolved within 3 weeks, suggesting microthrombi as the most likely aetiology. The child was clinically normal at the 3-month follow-up.…”

COVID-19–associated Coagulopathy

“…Accordingly, the cell-based model of hemostasis and whole blood viscoelastic and platelet function tests are more appropriate to mirror the pathophysiology of COVID-19–associated coagulopathy. 3 , 4 …”

Impact of COVID-19 on Future Ischemic Stroke Incidence

“…IS tends to occur in those with more medical comorbidities [ 10 ], but can also occur in patients without preconditions and/or under the age of 55 [ [11] , [12] , [13] ], suggesting even healthy people are at risk. COVID-19 is thought to lead to increased thrombotic events such as IS secondary to hypercoagulability caused by systemic inflammation, viral-induced endothelial damage and cardiac dysfunction [ 8 , [14] , [15] , [16] , [17] ]. Multiple studies report that most COVID-19 related IS are cryptogenic or embolic stroke of undetermined significance (ESUS), which is a stroke subtype thought to be caused mostly by an undiagnosed cardioembolic source [ 14 , 18 ].…”