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Mol Neurobiol. 2015 Dec;52(3):1572-1579. doi: 10.1007/s12035-014-8952-x. Epub 2014 Nov 4.

Hemorrhagic Transformation after Tissue Plasminogen Activator Reperfusion Therapy for Ischemic Stroke: Mechanisms, Models, and Biomarkers.

Author information

1
Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, People's Republic of China.
2
Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, 430060, People's Republic of China. chenqx666@sohu.com.
3
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, 720 Rutland Ave, Ross Bldg 370B, Baltimore, MD, 21205, USA. jwang79@jhmi.edu.

Abstract

Intracerebral hemorrhagic transformation (HT) is well recognized as a common cause of hemorrhage in patients with ischemic stroke. HT after acute ischemic stroke contributes to early mortality and adversely affects functional recovery. The risk of HT is especially high when patients receive thrombolytic reperfusion therapy with tissue plasminogen activator, the only available treatment for ischemic stroke. Although many important publications address preclinical models of ischemic stroke, there are no current recommendations regarding the conduct of research aimed at understanding the mechanisms and prediction of HT. In this review, we discuss the underlying mechanisms for HT after ischemic stroke, provide an overview of the models commonly used for the study of HT, and discuss biomarkers that might be used for the early detection of this challenging clinical problem.

KEYWORDS:

Blood-brain barrier; Hemorrhagic transformation; Ischemic stroke; Tissue plasminogen activator

PMID:
25367883
PMCID:
PMC4418959
DOI:
10.1007/s12035-014-8952-x
[Indexed for MEDLINE]
Free PMC Article

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