(Stroke. 2005;36:724.)
© 2005 American Heart Association, Inc.
Original Contributions |
UCSF Neurology, San Francisco, Calif
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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
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