Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment in Acute Ischemic Stroke

Hemorrhagic transformation (HT) is a common complication after thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) in ischemic stroke. In this article, recent research progress of HT in vivo and in vitro studies was reviewed. We have discussed new potential mechanisms and possible experimental models of HT development, as well as possible biomarkers and treatment methods. Meanwhile, we compared and analyzed rodent models, large animal models and in vitro BBB models of HT, and the limitations of these models were discussed. The molecular mechanism of HT was investigated in terms of BBB disruption, rt-PA neurotoxicity and the effect of neuroinflammation, matrix metalloproteinases, reactive oxygen species. The clinical features to predict HT were represented including blood biomarkers and clinical factors. Recent progress in neuroprotective strategies to improve HT after stroke treated with rt-PA is outlined. Further efforts need to be made to reduce the risk of HT after rt-PA therapy and improve the clinical prognosis of patients with ischemic stroke.

Automated summary

This article reviews the recent research progress on hemorrhagic transformation (HT) in ischemic stroke patients treated with thrombolysis. It discusses the mechanisms, experimental models, and biomarkers of HT, as well as the limitations of different models. Furthermore, it investigates the molecular mechanism and clinical features of HT, and outlines neuroprotective strategies to improve HT. The authors suggest further efforts to reduce the risk of HT and improve the clinical prognosis of patients treated with thrombolysis.