Increased platelet activation in the chronic phase after cerebral ischemiaand intracerebral hemorrhage

Background and Purpose-Enhanced thromboxane (TX) biosynthesis has previousl y been reported in the acute phase after ischemic stroke. We investigated w hether enhanced urinary excretion of 11-dehydro-TXB2, a noninvasive index o f platelet activation, was present in the chronic phase after a transient i schemic 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 e nzymatic metabolite of TXA(2), 11-dehydro-TXB2, was measured by a previousl y validated radioimmunoassay, The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases. Results-Urinary 11-dehydro-TXB2 averaged 294+/-139, 413+/-419, and 557+/-43 2 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracer ebral hemorrhage, respectively; the values were higher in all subgroups (P< 0.01) than that in control patients (119+/-66 pmol/mmol). increased 11-dehy dro-TXB2 excretion was present in 59% of all patients, in 60% (P<0.001) of patients with TIA, in 56% (P<0.001) of patients with ischemic stroke, and i n 73% (P<0.001) of patients with intracerebral hemorrhage, Atrial fibrillat ion, no aspirin use, and severity of symptoms at follow-up contributed inde pendently to the level of 11-dehydro-TXB2 excretion in a multiple linear re gression analysis. Conclusions-Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persist ent platelet activation, which is associated with atrial fibrillation and p oor stroke outcome, can be substantially suppressed by aspirin treatment.