Increased platelet activation in the chronic phase after cerebral ischemia and intracerebral hemorrhage.

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Abstract
Background and Purpose —Enhanced thromboxane (TX) biosynthesis has previously been reported in the acute phase after ischemic stroke. We investigated whether enhanced urinary excretion of 11-dehydro-TXB 2 , a noninvasive index of platelet activation, was present in the chronic phase after a transient ischemic attack (TIA) or stroke, including intracerebral hemorrhage. Methods —We obtained a single urinary sample from 92 patients between 3 and 9 months after onset of stroke or TIA. The urinary excretion of the major enzymatic metabolite of TXA 2 , 11-dehydro-TXB 2 , was measured by a previously validated radioimmunoassay. The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases. Results —Urinary 11-dehydro-TXB 2 averaged 294±139, 413±419, and 557±432 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracerebral hemorrhage, respectively; the values were higher in all subgroups ( P 2 excretion was present in 59% of all patients, in 60% ( P P P 2 excretion in a multiple linear regression analysis. Conclusions —Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persistent platelet activation, which is associated with atrial fibrillation and poor stroke outcome, can be substantially suppressed by aspirin treatment.

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