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Therapeutic strategies to attenuate hemorrhagic transformation after tissue plasminogen activator treatment for acute ischemic stroke
Author(s) -
Shimohata Takayoshi,
Kanazawa Masato,
Kawamura Kunio,
Takahashi Tetsuya,
Nishizawa Masatoyo
Publication year - 2013
Publication title -
neurology and clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
0ISSN - 2049-4173
DOI - 10.1111/ncn3.63
Subject(s) - medicine , tissue plasminogen activator , therapeutic effect , stroke (engine) , plasminogen activator , pharmacology , t plasminogen activator , ischemia , matrix metalloproteinase , ischemic stroke , mechanical engineering , engineering
Here, we describe a therapeutic strategy for attenuating hemorrhagic transformation (HT) after tissue plasminogen activator ( tPA ) treatment for acute ischemic stroke. Recent studies have shown that tPA treatment is beneficial within 4.5 h of onset for patients with acute ischemic stroke. However, the risk of serious or fatal symptomatic hemorrhage increases with delayed initiation of treatment. HT is considered to be caused by ischemic/reperfusion injury, as well as the toxicity of tPA itself. Therapeutic strategies to attenuate HT after tPA treatment might involve (i) identification of risk factors for HT after tPA treatment and (ii) the development of thrombolytic drugs, which are less likely to cause bleeding, or drugs that can be concomitantly administered for vascular protection. Several studies have shown that matrix metalloproteinases and free radicals are potential therapeutic targets. In addition, we recently showed that inhibition of the vascular endothelial growth factor (VEGF) signaling pathway might be a promising therapeutic strategy for attenuating HT after tPA treatment. Further studies are required to link the results obtained in experimental animal models to human clinical trials.