Thromb Haemost 1979; 41(03): 512-522
DOI: 10.1055/s-0038-1646803
Original Articles
Schattauer GmbH Stuttgart

Spontaneous Platelet Aggregation in Cerebrovascular Disease II

Further Characterisation of the Platelet Defect
E M G Hoogenduk
The Departments of Haematology and Neurology, University Hospital» Wilhelmina Gasthuis«, Amsterdam, The Netherlands
,
C S P Jenkins
The Departments of Haematology and Neurology, University Hospital» Wilhelmina Gasthuis«, Amsterdam, The Netherlands
,
E M van Wijk
The Departments of Haematology and Neurology, University Hospital» Wilhelmina Gasthuis«, Amsterdam, The Netherlands
,
J Vos
The Departments of Haematology and Neurology, University Hospital» Wilhelmina Gasthuis«, Amsterdam, The Netherlands
,
J W ten Cate
The Departments of Haematology and Neurology, University Hospital» Wilhelmina Gasthuis«, Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 29 April 1978

Accepted 27 July 1978

Publication Date:
09 July 2018 (online)

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Summary

A group of 186 patients with Transient Ischaemic Attacks (TIA) or cerebral Infarction (Cl) was found to demonstrate in vitro Spontaneous Platelet Aggregation (SPA) in 39% of those studied. Of the 176 normal subjects studied the incidence of in vitro SPA was found to be 5%. Further investigation of the phenomenon of SPA revealed that:

1. it is associated with ADP-hyperaggregability, i. e. the threshold concentration to induce second wave aggregation is decreased;

2. it is dependant on the increase in pH which occurs in platelet-rich plasma stirring in an aggregometer while concurrent ADP-hyperaggregability is independant of this change in pH;

3. it is associated with malondialdehyde production and the release of endogenous 5- hydroxytryptamine; and that

4. in addition Km and Vmax values for [14C]-5HT incorporation are normal; and that

5. no gross abnormalities of the platelet membrane glycoproteins were apparent although occasionally glycoprotein III was found to be increased.

This study demonstrates abnormal platelet behaviour in patients with TIA and Cl where the enzyme system involved in thromboxane production is sufficiently stimulated, by stirring alone, to induce aggregation of platelets and the release reaction.

Acetylsalicylic acid abolishes SPA and prolongs the bleeding time with similar characteristics as has been described for normal individuals. Plasma (3-thromboglobulin levels are significantly increased in the patients studied. However, no correlation was established with the incidence of in vitro SPA.