Coronavirus disease 2019-induced hypercoagulability and its clinical implications.
Asian Cardiovasc Thorac Ann
; 30(5): 515-523, 2022 Jun.
Article
in English
| MEDLINE | ID: covidwho-1582716
ABSTRACT
Coronavirus disease 2019 is the disease produced by severe acute respiratory syndrome-coronavirus-2, which is introduced into the host's cell thanks to the angiotensin-converting enzyme 2 receptor. Once there, it uses the cell's machinery to multiply itself. In this process, it generates an immune response that stimulates the lymphocytes to produce cytokines and reactive oxygen species that begin to deteriorate the endothelial cell. Complement activation, through the complement attack complex and C5a, contributes to this endothelial damage. The different mediators further promote the expression of adhesion molecules on the endothelial surface, which encourages all blood cells to adhere to the endothelial surface to form small conglomerates, called clots, which obstruct the lumen of the small blood vessels. Furthermore, the mediators of clot lysis are inhibited. All this promotes a prothrombotic environment within the pulmonary capillaries that is reflected in the elevation of D-dimer. The only solution for this cascade of events seems to be the implementation of an effective anticoagulation protocol that early counteracts the changes induced by thrombi in the pulmonary circulation and reflected in the functioning of the right ventricle.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Thrombosis
/
Thrombophilia
/
COVID-19
Type of study:
Diagnostic study
/
Prognostic study
Limits:
Humans
Language:
English
Journal:
Asian Cardiovasc Thorac Ann
Journal subject:
Vascular Diseases
/
Cardiology
Year:
2022
Document Type:
Article
Affiliation country:
02184923211069185
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