Abstract

Coronavirus disease 2019 (COVID-19), a respiratory syndrome, is a global pandemic. Therefore, there is an urgent need to explore mechanisms implicated in the pathogenesis of the disease. Clinical and autopsy studies show a complex chain of events preceding COVID-19-related death. The disease is characterized by endothelial dysfunction, platelet activation, thrombosis, coagulopathy, and multiple organ failure. Globally, millions of patients with coronary heart disease undergo percutaneous coronary intervention (PCI) each year. These patients undergo high-intensity antithrombotic therapy during hospitalization and dual antiplatelet therapy (DAPT) for at least 6 months post PCI. COVID-19 is characterized by changes in platelet counts. Treatment of ischemic events that occur during stent implantation is associated with bleeding complications in patients following PCI complicated by COVID-19. This review summarizes recent progress in activation status and levels of COVID-19-related platelet changes. These findings will provide information on the effectiveness of antithrombotic therapy for the management of platelet changes in COVID-19 patients.

Highlights

  • Coronavirus disease 2019 (COVID-19), a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is a worldwide pandemic

  • COVID-19 is associated with pneumonia and a wide range of effects on the cardiovascular system, it is a health and economic burden worldwide [2,3,4,5]

  • A recent study reports significant changes in platelet gene expression and function in COVID-19 patients. These changes result in platelet activation and aggregation, which are potential novel mechanisms for management of COVID-19-associated thrombosis and coagulopathy [15]

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Summary

INTRODUCTION

Coronavirus disease 2019 (COVID-19), a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is a worldwide pandemic. A recent study reports significant changes in platelet gene expression and function in COVID-19 patients These changes result in platelet activation and aggregation, which are potential novel mechanisms for management of COVID-19-associated thrombosis and coagulopathy [15]. Clinical studies on SARS patients reported an increase in activated partial thromboplastin time (42.8%), thrombocytopenia (44.8%), and elevated D-dimer (45.0%) [22]. A previous study reports thrombocytopenia in SARS patients (55%), increase in activated partial thromboplastin time (63%) and Abbreviations: ACS, acute coronary syndrome; ARDS, acute respiratory distress syndrome; COVID-19, coronavirus disease 2019; DAPT, dual antiplatelet therapy; DIC, disseminated intravascular coagulation; IL-6, interleukin-6; MOF, multiple organ failure; PCI, percutaneous coronary intervention; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; STEMI, ST-segment elevation myocardial infarction. Administration of low-molecular-weight heparin daily is preferred over unfractionated heparin, as it reduces personal protective equipment use and exposure of health care workers [25]

BRIEF SUMMARY OF VIRAL PNEUMONIA PATHOLOGY
Lung Pathology of Severe Acute Respiratory Syndrome
Endothelial Dysfunction
Platelet Activation and Depletion
Immune Defense and Cytokine Storms
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS
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