Related Experiment Video
Updated: Nov 21, 2025
A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
COVID‑19 and ischemic stroke: Mechanisms of hypercoagulability (Review)
Shuoqi Zhang1, Jinming Zhang2, Chunxu Wang2
1Department of Neurology, The Second Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Insights
Severe COVID-19 can cause acute ischemic stroke (AIS) by promoting hypercoagulability. This review explores the mechanisms linking COVID-19 infection to hypercoagulability and stroke, aiding treatment strategies.
Area of Science:
- Neurology
- Infectious Diseases
- Hematology
Background:
- The coronavirus disease 2019 (COVID-19) pandemic has been associated with severe complications, including acute ischemic stroke (AIS).
- Patients with severe COVID-19 and AIS often present with abnormal coagulation profiles, characterized by elevated D-dimer and fibrinogen levels, and thrombocytopenia.
- Existing research suggests a link between COVID-19 infection and a hypercoagulable state, increasing stroke risk, but the precise mechanisms remain elusive.
Purpose of the Study:
- To review current research on the relationship between COVID-19, hypercoagulability, and ischemic stroke.
- To elucidate the underlying mechanisms by which COVID-19 infection induces a hypercoagulable state.
- To identify potential therapeutic strategies targeting these mechanisms for improved patient outcomes and prevention of AIS.
Main Methods:
- Comprehensive literature review of studies investigating COVID-19, coagulation disorders, and ischemic stroke.
- Analysis of proposed pathophysiological pathways linking viral infection to hypercoagulability.
- Synthesis of current evidence on therapeutic interventions for COVID-19-associated hypercoagulability and stroke.
Main Results:
- COVID-19 infection is strongly associated with hypercoagulability, evidenced by specific laboratory markers.
- Several potential mechanisms are implicated, including endothelial dysfunction, complement activation, and direct viral effects on coagulation factors.
- Understanding these mechanisms is crucial for developing targeted treatments.
Conclusions:
- Hypercoagulability is a significant complication of severe COVID-19, contributing to AIS.
- Further research into the specific molecular pathways is needed to guide effective therapeutic interventions.
- Targeted anticoagulation and anti-inflammatory therapies may play a role in managing COVID-19-associated hypercoagulability and preventing stroke.
Abstract:
During the coronavirus disease 2019 (COVID‑19) pandemic, some patients with severe COVID‑19 exhibited complications such as acute ischemic stroke (AIS), which was closely associated with a poor prognosis. These patients often had an abnormal coagulation, namely, elevated levels of D‑dimer and fibrinogen, and a low platelet count. Certain studies have suggested that COVID‑19 induces AIS by promoting hypercoagulability. Nevertheless, the exact mechanisms through which COVID‑19 leads to a hypercoagulable state in infected patients remain unclear. Understanding the underlying mechanisms of hypercoagulability is of utmost importance for the effective treatment of these patients. The present review aims to summarize the current status of research on COVID‑19, hypercoagulability and ischemic stroke. The present review also aimed to shed light into the underlying mechanisms through which COVID‑19 induces hypercoagulability, and to provide therapies for different mechanisms for the more effective treatment of patients with COVID‑19 with ischemic stroke and prevent AIS during the COVID‑19 pandemic.
Related Concept Videos
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
01:30Venous Thrombosis I: Introduction
01:17Ischemic Heart Disease: Overview
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
01:20Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...