The following are key points to remember from this Perspective on Antiplatelet Therapy Following Percutaneous Coronary Intervention (PCI) in Patients Complicated by COVID-19 from the Tianjin Medical University General Hospital, Tianjin, China:

1. The worldwide pandemic caused by the novel acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a new and lethal disease termed coronavirus disease 2019 (COVID-19). Diffuse alveolar hemorrhage (DAH) has been reported as a common finding from lung pathology in COVID-19 patients, raising safety concerns regarding dual antiplatelet therapy (DAPT) on life-threatening bleeding complications among SARS-CoV-2 infected patients, especially the risk for DAH.
2. In addition to thrombosis and hemostasis, emerging evidence supports a putative role of platelets in host defense against infections, which add a greater layer of complexity in evaluating the role of antiplatelet therapy in the setting of viral pneumonia.
3. Early antiplatelet therapy, especially P2Y₁₂ antagonists, may be beneficial due to their inhibitory effects on platelet activation and generation of neutrophil-platelet aggregates, key mechanisms in both thrombus formation and pulmonary neutrophil recruitment. Three issues should be taken into account when interpreting the impact of antiplatelet therapy on disease progression.
4. First, the timing of administration: In the early phase of infection, platelet inhibition may reduce intravascular fibrin and thrombus formation, thereby preventing the ensuing consequences.
5. Second, the choice of oral P2Y₁₂ inhibitors: Despite the fact that all P2Y₁₂ inhibitors reduce platelet-leukocyte aggregates and platelet-derived pro-inflammatory cytokines from α-granules, ticagrelor is unique in having the only well-documented additional target of inhibition, the equilibrative nucleoside transporter 1 (ENT1), contributing to inhibition of cellular adenosine uptake. Therefore, ticagrelor confers more potent anti-inflammatory properties via dual inhibition of platelet P2Y₁₂ receptor and ENT1.
6. Third, the circulating platelet counts: Both primary (immune thrombocytopenia) and secondary (enhanced consumption) thrombocytopenia are associated with increased risk for infection (including pneumonia) and worsened clinical outcomes associated with acute respiratory distress syndrome. Individuals who are thrombocytopenic would lose the ability to deposit fibrinogen and fail to seal the damaged pulmonary vasculature.
7. To counterbalance increased bleeding risk associated with DAPT, emerging evidence supports a net benefit of aspirin-free strategies after PCI for patients at low, intermediate, and high risk for both ischemia and bleeding, which is mainly driven by the reduction in bleeding events. Specifically, this strategy reduces the duration of aspirin to 1-3 months while allowing for more prolonged use of potent P2Y₁₂ inhibitors. Based on available evidence, among patients currently on DAPT, maintaining P2Y₁₂ inhibitor monotherapy (preferably ticagrelor) may be scientifically reasonable for patients with PCI performed ≥3 months.
8. Due to the lack of robust evidence, for those with PCI performed <3 months, DAPT should NOT be discontinued.
9. The COVID-19 pandemic is currently a global disaster, but provides a unique opportunity to study the key questions concerning the preventive, therapeutic, or even aggravating effects of antiplatelet therapy on viral pneumonia based on real-world data.
10. At this time, clinicians need to be cognizant of the pros and cons of antiplatelet therapy in patients complicated by COVID-19 and individualize therapy based on risk of bleeding.

Clinical Topics: COVID-19 Hub, Dyslipidemia, Invasive Cardiovascular Angiography and Intervention, Prevention, Lipid Metabolism

Keywords: Adenosine, Aspirin, Blood Platelets, Coronavirus, COVID-19, Equilibrative Nucleoside Transporter 1, Fibrin, Hemorrhage, Hemostasis, Percutaneous Coronary Intervention, Platelet Aggregation Inhibitors, Pneumonia, Viral, Primary Prevention, Purinergic P2Y Receptor Antagonists, SARS Virus, Thrombocytopenia, Thrombosis

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