Circulation. 1999;100:e155
(Circulation. 1999;100:e155.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Direct Detection of Heparin-Induced Platelet Aggregation
T. Matsuo, MD;
K. Kario, MD
Hyogo Prefectural Awaji Hospital,
Sumoto, Japan
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Introduction
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To the Editor:
Enhanced platelet aggregation responses to stimulation with ADP or
thrombin receptor agonist peptides (TRAP) have been observed during
heparin therapy in patients with unstable angina. However, the
platelet aggregation curve in Figure 3 of the article by Xiao and
Théroux1 was not obtained from a direct detection to
evaluate heparin-induced hyperaggregation.
A new platelet aggregometer (AG-10; Kowa, Japan) that uses a
laser-light-scattering beam was introduced.2 Platelet
aggregates, the size of which was measured as total voltage of
light-scatter intensity at 1.0-second intervals for a 10-minute period,
were divided into 3 ranges: small aggregates (diameter 9 to 25
µm), medium (26 to 50 µm), and large (>50 µm). We
found that young smokers had an increased number of small platelet
aggregates, which cannot be detected with a conventional aggregometer
based on the turbidometric method.3 This device detects
platelet aggregation in the small-aggregate size range by the
addition of unfractionated heparin (UFH), and the aggregates are
disaggregable in incubation with protamine sulfate. When platelet
aggregation induced by UFH at a final concentration of 0.5 U/mL was
observed in 36 normal subjects with no history of heparin exposure, 13
had a positive response in excess of 0.5 V of light intensity in the
small-aggregate size range. In chronic hemodialysis patients in whom
heparin had been used regularly for many years, a positive response
with heparin-induced aggregates was noted in 37 of 59 patients, which
was increased compared with that of normal subjects. The light
intensity in the small-aggregate size range was enhanced during
heparinized dialysis. In patients with a positive heparin response, the
intensity of aggregates after heparin was significantly increased
compared with that in nonresponders to heparin. Also, we obtained the
same results by this system, that enhanced platelet aggregation
response to heparin was not inhibited by aspirin or argatroban but was
inhibited by anti-glycoprotein IIb/IIIa antibodies. The
findings of enhanced platelet aggregation during heparin infusion
in Figure 2 could be directly obtained without the addition of ADP or
TRAP using the new device. In addition, the subjects in the article by
Xiao and Théroux1 could likely have been classified
into 2 groups: responders and nonresponders to heparin. The authors
would have obtained clearer conclusions regarding the effect of heparin
on platelets in patients with unstable angina.
Direct detection of heparin-induced platelet aggregation may be a
useful method to evaluate the efficacy of heparin therapy in
coronary heart disease with enhanced platelet
aggregation.
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References
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Xiao Z, Théroux P. Platelet activation
with unfractionated heparin at therapeutic concentrations and
comparisons with a low-molecular-weight heparin and with a direct
thrombin inhibitor. Circulation. 1998;97:251–256.[Abstract/Free Full Text]
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Tohgi H, Takahashi H, Watanabe K, Kuki H, Shirasawa Y.
Development of large platelet aggregates from small aggregates as
determined by laser-light scattering: effects of aggregant
concentration and antiplatelet medication. Thromb
Haemost. 1996;75:838–843.[Medline]
[Order article via Infotrieve]
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Matsuo T, Koide M, Sakuramoto H, Matsuo M, Fuji K.
Small size of platelets aggregates detected by light scattering in
young habitual smokers. Thromb Haemost. 1997;71(suppl). 71.
Abstract.
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Introduction
References