TY - JOUR
T1 - Shear-induced platelet aggregation in cerebral ischemia
AU - Uchiyama, Shinichiro
AU - Yamazaki, Masako
AU - Maruyama, Shoichi
AU - Handa, Makoto
AU - Ikeda, Yasuo
AU - Fukuyama, Mayumi
AU - Itagaki, Ichiro
PY - 1994/8
Y1 - 1994/8
N2 - Background and Purpose Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents. Methods The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in titrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents. Results Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shearinduced platelet aggregation with platelet count, agonistinduced platelet aggregation, fibrinogen level, or 0-thrombo-globulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it. Conclusions These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the incre.
AB - Background and Purpose Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents. Methods The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in titrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents. Results Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shearinduced platelet aggregation with platelet count, agonistinduced platelet aggregation, fibrinogen level, or 0-thrombo-globulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it. Conclusions These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the incre.
KW - Cerebral ischemia
KW - Platelet aggregation
KW - Thrombosis
KW - Ticlopidine
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U2 - 10.1161/01.STR.25.8.1547
DO - 10.1161/01.STR.25.8.1547
M3 - Article
C2 - 8042205
AN - SCOPUS:0028059351
VL - 25
SP - 1547
EP - 1551
JO - Stroke
JF - Stroke
SN - 0039-2499
IS - 8
ER -