THROMBOEMBOLIC EVENTS ASSOCIATED WITH COVID-19: LITERATURE REVIEW ON PATHOPHYSIOLOGICAL MECHANISMS AND GENETIC PREDISPOSITION
DOI:
https://doi.org/10.56238/levv16n55-145Keywords:
COVID-19, SARS-CoV-2, Thromboembolic Events, Blood Coagulation, Genetic PredispositionAbstract
Introduction: SARS-CoV-2 infection, initially recognized as a respiratory disease, has proven to be a systemic condition associated with significant hemostatic changes, with a significant increase in the incidence of thromboembolic events. Evidence suggests that these complications result from a complex interaction between systemic inflammation, endothelial dysfunction, and dysregulated activation of the coagulation cascade, which can occur even in individuals without previously identified thrombotic risk factors. General objective: The present study aims to analyze the relationship between SARS-CoV-2 infection and the occurrence of thromboembolic events, with an emphasis on the possible contribution of genetic factors associated with thrombotic predisposition in the post-COVID-19 period. Methodology: This is an observational, descriptive study with a qualitative and quantitative approach, developed from a structured narrative review of the literature in national and international databases, Scielo and PubMed, using scientific articles published mainly in the last 4 years, using as an inclusion criterion the association between SARS-CoV-2 infection and thromboembolic events. Results: The results of the literature demonstrate a consistent association between COVID-19 and an increase in venous and arterial thromboembolic events, accompanied by laboratory changes indicative of hypercoagulability, such as elevated D-dimer and inflammatory markers. In addition, studies suggest that genetic polymorphisms related to coagulation and fibrinolysis may act as individual modulators of thrombotic risk, contributing to the observed clinical variability. Conclusion: It is concluded that thrombosis associated with COVID-19 has a multifactorial etiology, involving inflammatory, endothelial, and genetic mechanisms. Integrated investigation of these factors may aid in risk stratification and the development of more individualized preventive and therapeutic strategies, reinforcing the need for future studies with greater methodological robustness to elucidate the role of genetic predisposition in the post-COVID-19 context.
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