CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 2, May/June 2023 116 AFRICA inflammatory process has been reported since the onset of the disease. Pathophysiological mechanisms such as inflammation, immobilisation and endothelial dysfunction have been reported to be involved in the formation of the condition.5 A post-viral infection is triggered by massive macrophage activation that creates a cytokine storm.1,6 An inflammatory process is triggered by the viral infection, and the thrombotic process can accelerate after macrophage activation.6 Although pulmonary embolism is the most common thrombotic disease in patients with COVID-19, arterial thrombosis occurs less frequently but occurs more frequently as a morbid complication. The incidence of venous thromboembolism during COVID-19 infection has been reported to reach as high as 25%, and arterial vascular events can occur at a frequency of up to 4%.7,8 Coagulopathy leads to a high mortality rate and laboratory abnormalities such as an elevated D-dimer level are important markers.3,4,9 The time of the onset of thrombosis is still unknown. Some studies have reported that it can occur between five and 25 days after the onset of COVID-19.2,10,11 In addition, high levels of lymphopaenia, D-dimer and ferritin have been shown as poor prognosis markers in these patients. In our patient, thrombosis emerged on the seventh day and showed markers of poor prognosis. In this report, we present the lung pathology and aortic thrombotic condition associated with the development of COVID-19 infection in a middle-aged patient without any additional disease. A likely association has been reported between COVID-19 infection and the development of an intense prothrombotic state that could lead to significant arterial complications, which should be avoided. Cases of thrombosis in medium and large arterial vessels have also been reported, albeit rarely.12,13 A worldwide consensus has been reached on the use of low-molecular-weight heparins in patients with COVID-19 to prevent or control the thrombotic process.6-8 However, pulmonary embolic and vascular thrombotic occlusions have been reported, even during heparin treatment. The general trend in this situation is the degree of vascular occlusion and the presence of ischaemic changes in the extremities. Surgical thrombectomy, intra-arterial thrombolysis, peripheral arterial catheter-directed thrombolysis and thrombolytic therapy were used in cases with intravascular thrombi and ischaemic symptoms,14 as in our case. As non-invasive applications were not performed in our hospital, our patient was surgically treated with embolectomy from the femoral arteries. Conclusions COVID-19 infection, which can show intense hypercoagulation, may cause thrombotic events, even in patients with no atherosclerotic tendency in their vascular structures. Even in the absence of a previous vascular problem or a risk factor such as atrial fibrillation, all patients should be closely monitored for this catastrophic and distressing clinical feature. Vascular system examination has become highly important, especially in the follow up of in-patients. In addition, it is considered useful in warning against the possible occurrence of sudden symptoms so that they are not overlooked in out-patients. References 1. Watanabe M. The COVID-19 pandemic in Japan. Surg Today 2020; 50(8): 787–793. 2. Bresadola V, Biddau C, Puggioni A, Tel A, Robiony M, Hodgkinson J, Leo CA. General surgery and COVID-19: review of practical recommendations in the first pandemic phase. Surg Today 2020; 50(10): 1159–1167. 3. Guan W, Ni Z, Hu Y, et al. China Medical Treatment Expert Group for Covid-19. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med 2020; 382: 1708–1720. 4. Yang X, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a singlecentered, retrospective, observational study. Lancet Respir Med 2020; 8(5): 475–481. 5. Bikdeli B, Madhavan MV, Jimenez D, et al. COVID-19 and thrombotic or thromboembolic disease: implications for prevention, antithrombotic therapy, and follow-up. J Am Coll Cardiol 2020; 75: 2950e73. 6. McGonagle D, Sharif K, O’Regan A, Bridgewood C. The role of cytokines including interleukin-6 in COVID-19 induced pneumonia and macrophage activation syndrome-like disease. Autoimmun Rev 2020; 19: 10253. 7. Bompard F, Monnier H, Saab I. Pulmonary embolism in patients with COVID-19 pneumonia. Eur Respir J 2020; 56: 2001365. 8. Klok FA, Kruip MJ, van der Meer NJ. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020; 191: 145–147. 9. Casella IB. Physiopathology of SARS-CoV-2-infection-associated thrombosis. J Vasc Bras 2020; 19: e20200128. 10. Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost 2020; 18(4): 844–847. 11. Zhang Y, Xiao M, Zhang S, et al. Coagulopathy and antiphospholipid antibodies in patients with Covid-19. N Engl J Med 2020; 382(17): e38. 12. Gomez-Arbelaez D, Ibarra-Sanchez G, Garcia-Gutierrez A, ComangesYeboles A, Ansuategui-Vicente M, Gonzalez-Fajardo JA. COVID-19 Related aortic thrombosis: A report of four cases. Ann Vasc Surg 2020; 67: 10–13. 13. Baeza C, González A, Torres P, Pizzamiglio M, Arribas A, Aparicio C. 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