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(Stroke. 2004;35:2498.)
© 2004 American Heart Association, Inc.
Original Contributions |
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
There is overwhelming evidence that hyperglycemia is detrimental in cerebral ischemia, not only from experimental research but also from an increasing number of clinical studies.1,2 Elevated admission glucose levels are associated with increased mortality and worse functional outcome from ischemic stroke.3,4 In human magnetic resonance imaging studies, tissue at risk will progress to infarction in the presence of high blood glucose level, and diffusion-weighted imaging lesion will grow even in recanalized patients receiving thrombolytic therapy.57 The mechanisms of hyperglycemic cellular injury have been largely clarified.8 Although experimental ischemic damage is made worse by hyperglycemia and reduced by lowering the blood glucose level, the therapeutic effect of rapidly acting insulin still remains to be proven in clinical trials.8
This article complements the original observation published last year by the same group: the deleterious effect of hyperglycemia depends on reperfusion in patients receiving recombinant tissue plasminogen activator (rtPA) treatment.9 Moderately elevated admission blood glucose (>140 mg/dL) emerged as the only independent predictor of poor outcome in patients recanalized by rtPA when controlled for stroke severity.
Also in a re-analysis of the National Institute for Neurological Disorders (NINDS) rtPA Trial, increased admission blood glucose level was independently associated with decreased odds for neurological improvement and the risk of symptomatic intracerebal hemorrhage was increased by 75% per each 100 mg/dL of blood glucose.3
In accordance with these studies, the data from Helsinki showed an increased risk of hemorrhagic change by 42% per each mmol/L of admission blood glucose in a logistic regression model.10
This
Related Article:
Stroke 2004 35: 2493-2498.
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