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No-Go to Tissue Plasminogen Activator for Transient Ischemic Attack
Author(s) -
David S. Liebeskind
Publication year - 2010
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.110.596023
Subject(s) - medicine , thrombolysis , tissue plasminogen activator , ischemia , occlusion , cardiology , middle cerebral artery , magnetic resonance imaging , stroke (engine) , brain ischemia , anesthesia , radiology , mechanical engineering , myocardial infarction , engineering
Thrombolysis is not a rational or evidence-based therapeutic option for transient ischemia, irrespective of vascular status. Even with overt middle cerebral artery (MCA) occlusion, complete resolution of symptoms during evaluation does not warrant intravenous tissue plasminogen activator. Symptom resolution may result from head-down positioning with improved hemodynamics, and rapid improvement remains one of the most common reasons cited for withholding thrombolysis.1,2 Multimodal computed tomography and magnetic resonance imaging have since enabled clinicians to rapidly depict proximal arterial occlusion, tissue status, and perfusion through the brain. Identification of an MCA occlusion, however, dangles an elusive carrot that may incite harm with unnecessary thrombolysis.The prevailing obsession with arterial occlusion has erroneously focused attention on clots rather than ischemia. Hemodynamic insufficiency, and not clots, causes symptoms when collaterals falter.3 The persistence of thrombolysis as the sole treatment for acute ischemic stroke perpetuates the notion that occlusion is a red flag for intervention, yet collaterals may offset or dissipate symptoms, even in proximal arterial …

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