Scoping review about pathogenesis, risk factors, and treatment of venous and arterial thrombosis in Coronavirus infection

Diana Malaeb^1*Sara Mansour^2*Chadia Haddad^3,4,5Nada Dia²Nada M Kassem^6*Mariam Dabbous²Ola Ahmad¹Farah Adel¹May Gamal¹Jisha Myalil Lucca¹Sami El Khatib^7,8Pascale Salameh^10,11,3,9Souheil Hallit^12,13,14Hassan Hosseini^15,16

• ¹Gulf Medical University, Ajman, United Arab Emirates
• ²Lebanese International University School of Pharmacy, Beqaa Governorate, Lebanon
• ³Institut National de Sante Publique d'Epidemiologie Clinique et de Toxicologie, Beirut, Lebanon
• ⁴Lebanese American University, Beirut, Lebanon
• ⁵Hopital Psychiatrique de la Croix, Jal El Dib, Lebanon
• ⁶Department of Biological and Chemical Sciences, Lebanese International University, Beirut, Lebanon
• ⁷Lebanese International University, Beqaa Governorate, Lebanon
• ⁸Gulf University for Science & Technology, Hawally, Kuwait
• ⁹Lebanese American University School of Medicine, Byblos, Lebanon
• ¹⁰Universite Libanaise Faculte des Sciences Medicales, Dekwaneh, Lebanon
• ¹¹University of Nicosia Medical School, Nicosia, Cyprus
• ¹²Universite Saint-Esprit de Kaslik Faculte de Medicine et des Sciences Medicales, Jounieh, Lebanon
• ¹³Effat University, Jeddah, Saudi Arabia
• ¹⁴ASU, Amman, Jordan
• ¹⁵Universite Paris-Est Creteil Val de Marne, Créteil, France
• ¹⁶Hopital prive Paul d'Egine, Champigny-sur-Marne, France

Introduction Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is now understood as a systemic illness marked by a distinctive coagulopathy that extends beyond its primary respiratory manifestations. Direct viral injury to the endothelium and an exaggerated inflammatory "cytokine storm" and complement activation disrupt normal hemostasis and create a prothrombotic environment. This scoping review aims to synthesize and compare the mechanisms, risk factors, and antithrombotic strategies associated with venous and arterial thrombosis in COVID-19. Methods A scoping review of English-language studies indexed in PubMed/Medline, OVID, and Wiley Library was conducted from January 2020 to June 2024. Search terms related to COVID-19, thrombotic complications, pathophysiological mechanisms, and antithrombotic therapies were included. Clinical trials, cohort and retrospective observational studies, systematic reviews, meta-analyses, and case reports are included. Two reviewers independently screened titles, abstracts, and full texts for relevance and extracted data to map current evidence on venous and arterial thrombosis in COVID-19. Results COVID-19-related coagulation problems can cause both venous and arterial thrombosis. Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, occurs in about 4 to 15 % of hospitalized patients and can increase to 30 % in those in intensive care, even with standard prevention. Elevated D-dimer levels are strongly associated with a higher risk of clot formation. Arterial clots, like strokes or heart damage, are less common but generally more serious, caused by platelet activation, inflammation, and small vessel blockage rather than just slow blood flow in veins. Evidence indicates that low-molecular-weight heparin is the preferred anticoagulant because it reduces both inflammation and clotting. Therapeutic doses may be especially beneficial for high-risk patients, and continuing clot prevention after hospital discharge helps lower the risk of late clots without significantly increasing bleeding risk. Conclusion Recognition of COVID-19–associated coagulopathy underscores the necessity of early risk stratification and individualized anticoagulation to mitigate thrombotic events and improve outcomes. Extended post-discharge prophylaxis appears promising in reducing late thrombotic complications. Future research should aim to refine optimal anticoagulant regimens and determine ideal prophylaxis duration for COVID-19–related thrombosis to reduce morbidity and mortality rates.