(Circulation. 1999;99:608-613.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Enhanced Shear-Induced Platelet Aggregation in Acute Myocardial Infarction
From the Division of Cardiology (S.G., H.S., M.G., M.O., S.H.), Department of Medicine, Tokai University School of Medicine, Kanagawa, Japan; Department of Medicine (Y.I.), Keio University School of Medicine, Tokyo, Japan; and Roon Research Center for Arteriosclerosis and Thrombosis (Z.M.R.), Departments of Molecular and Experimental Medicine and of Vascular Biology, The Scripps Research Institute, La Jolla, Calif.
Correspondence to Shinya Goto, MD, Division of Cardiology, Department of Medicine, Tokai University School of Medicine, Boseidai, Isehara, Kanagawa 259-11, Japan. E-mail shinichi{at}is.icc.u-tokai.ac.jp
Background—Experiments under
controlled flow conditions indicate that the binding of von
Willebrand factor (vWF) to platelet
glycoprotein (GP) Ib
and integrin
IIbß3 (GP IIb/IIIa complex) is crucial for
aggregation at elevated shear rates. We have tested how the plasma of
patients with acute myocardial infarction affects this
process.
Methods and Results—Citrated plasma was obtained from 18 patients
with acute myocardial infarction within 6 hours from the onset of
symptoms and from 26 control subjects with chest pain syndrome without
evidence of ischemia. Aggregation of normal platelets at
high shear rates was significantly greater in the presence of patient
than control plasma and was inhibited by both anti-GP Ib and
anti-IIbß3 monoclonal antibodies. The
observed values (mean±SD) were 47.6±17.8% versus 30.1±9.9% at
10 800 s-1 (P<0.01) and 32.9±14.1%
versus 17.5±9.5% at 7200 s-1 (P<0.01),
respectively, and were positively correlated with plasma vWF antigen
levels and ristocetin cofactor activities. In contrast, at the lower
shear rate of 1200 s-1, aggregation was similar in the
presence of control or patient plasma and was not inhibited by the
anti-GP Ib antibody. Both vWF antigen and platelet aggregation
decreased 2 weeks after the onset of myocardial infarction.
Conclusions—Shear-induced platelet aggregation is enhanced in plasma in the presence of acute myocardial infarction, apparently as a result of increased vWF concentration. This may contribute to the onset of acute coronary artery thrombosis and early reocclusion after reperfusion treatment.
Key Words: platelets • von Willebrand factor • glycoproteins • thrombosis
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