COVID-19 and Major Organ Thromboembolism: Manifestations in Neurovascular and Cardiovascular Systems

Abstract

COVID-19, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been shown to cause multisystemic damage. We undertook a systematic literature review and comprehensive analysis of a total of 55 articles on arterial and venous thromboembolism in COVID-19 and articles on previous pandemics with respect to thromboembolism and compared the similarities and differences between them. The presence of thrombosis in multiple organ systems points to thromboembolism being an integral component in the pathogenesis of this disease. Thromboembolism is likely to be the main player in the morbidity and mortality of COVID -19 in which the pulmonary system is most severely affected. We also hypothesize that D-dimer values could be used as an early marker for prognostication of disease as it has been seen to be raised even in the pre-symptomatic stage. This further strengthens the notion that thromboembolism prevention is necessary. We also examined literature on the neurovascular and cardiovascular systems, as the manifestation of thromboembolic phenomenon in these two systems varied, suggesting different pathophysiology of damage. Further research into the role of thromboembolism in COVID-19 is important to advance the understanding of the virus, its effects and to tailor treatment accordingly to prevent further casualties from this pandemic.

Keywords: COVID-19; Cardiovascular disease; D-dimer; Immunothrombosis; Neurovascular disease; Thromboembolism.

Fig. 1

The blue background (A) illustrates an outline of the coagulation cascade with its end result of thrombus formation and counter-regulatory fibrinolysis via plasmin activation which strikes a haemostatic balance between clotting and bleeding. Note that the thrombus/cross-linked fibrin breakdown results in fibrin degradation products and D-dimer, which is seen early in COVID-19. The pink background (B) illustrates the dysregulation of thrombosis and fibrinolysis which results in excessive thrombosis followed by haemorrhage known as disseminated intravascular coagulation.

Fig. 2

This figure illustrates the different mechanisms postulated for myocardial injury in COVID-19.