A Review on Molecular Mechanisms of Reocclusion Following Thrombolytic Therapy in Ischemic Stroke Patients
Stroke is the second most common cause of death worldwide. Despite many advances in the field of vascular neurology, intravenous (IV) tissue plasminogen activator (tPA) remains the only approved treatment for acute ischemic stroke, even though complication risk such as hypofibrinolysis and reocclusion, are reported in as high as 25-34% of cases. The exact mechanisms of unsuccessful thrombolytic therapy are unclear. Some molecular events such as activation of intrinsic and extrinsic pathways C-reactive protein (CRP), thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1) are the main causes of failure. Moreover, release of thrombin after tPA therapy, tissue factor pathway inhibitor (TFPI) inhibition, and some of gene polymorphisms may play a crucial role in reocclusion. Due to the necessity for development of effective strategies to improve clinical efficacy of tPA therapy, we aimed to evaluate the possible mechanisms, which may be responsible for re-occlusive complications after tPA therapy.
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