In-stent Thrombosis and COVID-19 Infection: Current Insights on the Mechanistic Relationship

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been demonstrated as a major risk factor in inducing coronary stent thrombosis due to its propensity to create a pro-thrombotic state. This review explores the mechanisms that may contribute to the increased thrombosis risk seen in COVID-19. Furthermore, we discuss the patient and haematological factors that predispose to an increased risk of stent thrombosis, as well as the role of certain antiplatelet and anticoagulation therapies, including ticagrelor and enoxaparin, that may reduce the likelihood and severity of in-stent thrombosis, in SARS-CoV-2 infection. To counter the proinflammatory and pro-thrombotic state shown in COVID-19, anti-thrombotic therapy in the future may be optimised using point-of-care platelet inhibition testing and inflammation-modifying therapies. Large-scale randomised trials with long-term follow-up are increasingly necessary to assess the intersection of COVID-19 and stent optimisation as well as the reduction of stent thrombosis after drug-eluting stent (DES) implantation.

Keywords: COVID-19; Stent thrombosis; anti-thrombotic therapy; antiplatelet; coronary artery disease; drug-eluting stent implantation.

Fig. (1)

COVID-19 thrombogenic pathways. Many of these pathways show strong inter-dependence and auto-amplification. Abbreviations: ACE2, angiotensin-converting enzyme 2; Ang II, angiotensin II, β-TG, beta thromboglobulin; IL, interleukin; MAS, macrophage activation syndrome; MASP-1, mannose binding lectin-associated serine protease; NK-cell, natural killer cell; NF-κB, nuclear factor kappa B; PAI-1, plasminogen activator inhibitor 1; PF4, platelet factor 4; RAS, renin-angiotensin system; ROS, reactive oxygen species; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TNF-α, tumour necrosis factor alpha.