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Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
Immunothrombosis: Bridging endothelial dysfunction and no-reflow in ischemic stroke
1Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Hypoxia Conditioning Translational Laboratory of Clinical Medicine, Chinese Institutes for Medical Research, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China.
The successful clinical treatment of acute ischemic stroke pivots on reestablishing blood flow. After attempting recanalization, the "no-reflow" phenomenon undermines the long-term benefits of clot-busting strategies, including thrombolytic and intravascular thrombectomy. A key pathological driver of this phenomenon is immunothrombosis, a specialized form of microthrombosis characterized by the aberrant aggregation of platelets with neutrophils and subsequent microvascular clot formation. The immunothrombotic process may be initiated or promoted by brain ischemia-induced endothelial inflammation. In this commentary, we elaborate on the mechanisms underlying the role of endothelial inflammation in the no-reflow cascade, and we recommend targeting immunothrombosis to mitigate no-reflow and optimize stroke management.
The successful clinical treatment of acute ischemic stroke pivots on reestablishing blood flow. After attempting recanalization, the "no-reflow" phenomenon undermines the long-term benefits of clot-busting strategies, including thrombolytic and intravascular thrombectomy. A key pathological driver of this phenomenon is immunothrombosis, a specialized form of microthrombosis characterized by the aberrant aggregation of platelets with neutrophils and subsequent microvascular clot formation. The immunothrombotic process may be initiated or promoted by brain ischemia-induced endothelial inflammation. In this commentary, we elaborate on the mechanisms underlying the role of endothelial inflammation in the no-reflow cascade, and we recommend targeting immunothrombosis to mitigate no-reflow and optimize stroke management.
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