(Stroke. 2005;36:724.)
© 2005 American Heart Association, Inc.
Original Contributions |
UCSF Neurology, San Francisco, Calif
A series of recent studieswith the one by Kleindorfer et al1 being a particularly good onedemonstrate that transient ischemic attacks (TIAs) are far from benign, especially in the short-term. Most recent studies report risk of stroke >10% in the 90 days after a TIA,25 as demonstrated here. These event rates are higher than those reported in older studies, likely because previous studies missed strokes that occurred during the first few days after a TIA, when the risk is particularly high.
The short-term event rates after TIA are generally higher than those reported from most studies of stroke after an initial ischemic stroke, indicating that TIA is a particularly unstable condition. One possible explanation is that the initial recovery identifies tissue still at risk.6 For example, if a ruptured plaque is responsible for the event, it remains thrombogenic after TIA, thereby generating a high risk of further ischemia. If the ruptured plaque initially produces a stroke rather than a TIA, it is less likely that the plaque will produce further symptoms: The adjacent vessel may remain occluded or the distal tissue may already be infarcted and not affected by further hypoperfusion or embolus.
A leisurely outpatient evaluation for TIA seems inappropriate in light of this instability. The risk of stroke in the first 48 hours after a TIA is
5%.2 This is actually greater than the risk of myocardial infarction in patients presenting with acute chest pain,7 and emergent evaluation of chest pain is standard of care.
One argument for not recommending an emergent evaluation after TIA has been that there is nothing to do to prevent a subsequent stroke. Although there are no completed large-scale trials of emergent therapies for TIA, most proven agents for secondary prophylaxis are expected to be effective in the short-term.8 Also, the risk of stroke after TIA is particularly high in those with carotid stenosis.4 The benefits of therapy are greater if endarterectomy is performed sooner after the initial ischemic event and complications are no more frequent,9,10 so carotid imaging should be performed immediately and endarterectomy should follow without delay in appropriate candidates. Finally, close monitoring of those presenting with an acute TIA should provide a greater opportunity to use tissue plasminogen activator in those with stroke afterward.11 Although emergent evaluation, treatment, and monitoring are expensive, the high short-term risk and substantial cost of stroke are likely to justify very aggressive care.
Every stroke after a TIA is a failure. Sometimes it is a failure of clinicians to use proven therapies. More frequently, it is a failure of researchers to establish effective proven therapies for TIA. We all have more work to do in this area; the opportunity is just too great.
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J. E Bray, K. Coughlan, and C. Bladin Can the ABCD Score be dichotomised to identify high-risk patients with transient ischaemic attack in the emergency department? Emerg. Med. J., February 1, 2007; 24(2): 92 - 95. [Abstract] [Full Text] [PDF] |
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