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Platelet activation in the cerebral circulation in different subtypes of ischemic stroke and Binswanger's disease
T Iwamoto1, H Kubo, M Takasaki
1Department of Geriatric Medicine, Tokyo Medical College Hospital.
Background And Purpose:
The sites of platelet activation in ischemic stroke are still unclear because previous reports have not identified them and various factors accompanied by stroke can activate platelets. We therefore examined the sites of platelet activation in patients with various types of ischemic stroke.
Methods:
The ratio of the plasma concentration of beta-thromboglobulin (BTG) in the internal jugular vein to that in the antecubital vein (BTG-B) was calculated as an indicator of platelet activation in the cerebral circulation. Plasma BTG concentration was determined in 75 control subjects and in 186 patients with various subtypes of ischemic stroke including lacunar, atherothrombotic, and cardioembolic strokes, transient ischemic attacks, and Binswanger's disease. The BTG ratio was evaluated with regard to subtype of stroke, time of blood sampling, size of infarct, presence of vascular lesions, and the effect of ticlopidine administration.
Results:
The mean BTG ratio was increased even in the chronic phase of most subtypes of stroke with the exception of cardioembolic stroke, which exhibited a persistent elevation of BTG-B concentrations. Patients with Binswanger's disease showed a significant (P < .01) and frequent elevation of BTG ratio. High BTG ratios occurred in cases with vascular lesions observed on cerebral angiography. There was no correlation between the BTG ratio and infarct size. Use of ticlopidine was partially associated with a lower BTG ratio.
Conclusions:
Platelets were activated in the cerebral circulation of patients with stroke even in the chronic phase, which suggests the development of underlying vascular lesions and of thrombogenesis with or without infarction. Platelets were activated mainly within the heart in cases of cardioembolic stroke. An enhanced release reaction secondary to platelet activation was often seen in patients with Binswanger's disease, which indicates that its pathophysiology differs from that of other subtypes of stroke.