Coronary Stent Thrombosis in COVID-19 Patients: A Systematic Review of Cases Reported Worldwide.

Wojciech Jan Skorupski,Marek Grygier,Marta Kałużna-Oleksy,Maciej Lesiak

doi:10.3390/v14020260

Wojciech Jan Skorupski, Marek Grygier + Show 2 more

Open Access

https://doi.org/10.3390/v14020260

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Abstract

Approximately 5 million percutaneous coronary interventions are performed worldwide annually. Therefore, stent-related complications pose a serious public health concern. Stent thrombosis, although rare, is usually catastrophic, often associated with extensive myocardial infarction or death. Because little progress has been made in outcomes following stent thrombosis, ongoing research is focusing on further understanding the predictors as well as frequency and timing in various patient subgroups. Coronavirus disease-2019 (COVID-19), a viral illness caused by the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), activates inflammatory mechanisms that potentially create a prothrombotic environment and increases the risk of local micro thromboembolism and all types of stent thrombosis. In-stent thrombosis occurrence increased during the COVID-19 pandemic, however, there is still lack of comprehensive studies describing this population. This review and worldwide analysis of coronary stent thrombosis cases related to COVID-19 summarizes all available data.

Highlights

5 million percutaneous coronary interventions (PCI) are performed worldwide annually
In-stent thrombosis could potentially be a consequence of the larger thrombus burden and specific mechanisms associated with plaque disruption among SARS-CoV-2 positive patients, which could lead to an increased risk of thrombus formation and coronary thrombotic complications [14,19]
We present the biggest worldwide analysis and review of coronary stent thrombosis cases related to COVID-19

Summary

Introduction

5 million percutaneous coronary interventions (PCI) are performed worldwide annually. The inflammatory pathophysiological mechanisms causing plaque rupture and the production of a prothrombotic environment may potentially increase the risk of local micro thromboembolism, may impair reperfusion, and increase the risk of coronary in-stent thrombosis [17]. This effect is due to a COVID-19 cytokine storm resulting from an imbalance in T-cell activation with dysregulated release of interleukin (IL)-6, IL-17, and other cytokines [14]. In-stent thrombosis could potentially be a consequence of the larger thrombus burden and specific mechanisms associated with plaque disruption among SARS-CoV-2 positive patients, which could lead to an increased risk of thrombus formation and coronary thrombotic complications [14,19]

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Conclusion