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Anticoagulation versus Antiplatelet Therapy in COVID-19-Related Stroke: Navigating Clinical Dilemmas in a Critically
Bo-Ying Huang1, Kuan-Hung Lin2, Kuan-Hsien Lu2
1Department of Neurology, Chi Mei Medical Center, Chiali, Tainan, Taiwan.
Insights
COVID-19-related stroke in cirrhosis patients presents a treatment challenge. A mechanism-guided approach, considering thromboinflammation and bleeding risk, is crucial for therapy selection over standard antiplatelet or anticoagulant use.
Area of Science:
- Neurology
- Infectious Diseases
- Hepatology
Background:
- Coronavirus disease 2019 (COVID-19) can trigger thromboembolic events, including stroke.
- Cirrhosis patients have a complex bleeding and clotting risk profile, further complicated by COVID-19.
- Standard stroke treatment guidelines may not apply to COVID-19-related thromboinflammatory strokes in cirrhosis.
Introduction:
The aim of this was to illustrate the treatment dilemma when coronavirus disease 2019 (COVID-19)-related thromboinflammatory stroke occurs in a patient with cirrhosis and to highlight a mechanism-guided framework for choosing between antiplatelet and anticoagulant therapy.
Case Presentation:
A 75-year-old man with alcoholic cirrhosis and esophageal varices was hospitalized for severe COVID-19 pneumonia. Because his D-dimer exceeded 3,000 ng/mL, prophylactic low-molecular-weight heparin (LMWH) was started. On day 4, he developed an acute right middle cerebral artery M2 occlusion (Alberta Stroke Program Early CT Score, ASPECTS 4); reperfusion therapy was contraindicated. A multidisciplinary team opted to continue LMWH and withhold antiplatelet agents, reasoning that thromboinflammation - not atherosclerosis - was the likely mechanism and that variceal bleeding risk was high. Acute kidney injury emerged on day 6, but careful monitoring showed neither hemorrhage nor stroke progression. The patient later died from respiratory failure unrelated to the stroke.
Conclusion:
In COVID-19 stroke with cirrhosis, guideline antiplatelet therapy may not fit the underlying biology. Treatment should be mechanism-guided, biomarker-informed, and adjusted to individual bleeding risk.
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