Thromb Haemost 1978; 40(01): 066-074
DOI: 10.1055/s-0038-1648635
Original Article
Schattauer GmbH Stuttgart

Thromboxane Generation and Platelet Aggregation in Survivals of Myocardial Infarction

A Szczeklik
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
,
R J Gryglewski
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
,
J Musiał
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
,
L Grodzińska
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
,
M Serwońska
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
,
E Marcinkiewicz
The Copernicus Academy of Medicine, Institute of Internal Medicine and Department of Pharmacology, Kraków, Poland
› Author Affiliations
Further Information

Publication History

Received 11 August 1977

Accepted 09 January 1978

Publication Date:
12 July 2018 (online)

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Summary

Arachidonic acid (AA)-induced platelet aggregation was studied in platelet-rich plasma of 30 male patients who survived myocardial infarction and in 30 healthy men of similar age. Mean platelet aggregation thresholds to A A were 746 ± 62 μM, and 869 ± 57 μM, respectively. Only in 2 healthy subjects, but in 12 patients, irreversible platelet aggregation was induced consistently with low concentrations of AA, under 500 μM. The rate of conversion of AA to thromboxane A2 (TXA2) by platelets of these patients was augmented. Furthermore, less endogenous TXA2 was required to trigger aggregation of their platelets as compared to the controls. We have also shown that in platelet-poor plasma of these patients with “hyperreactive” platelets there exists a transferable factor which makes platelets of healthy subjects more prone to aggregatory action of AA.

It is proposed that the assessment of platelet aggregability with AA provides a tool for identifying a subgroup of patients with coronary heart disease who might substantially benefit from the secondary preventive treatment with aspirin and with other antiplatelet drugs which inhibit the generation of TXA2 in platelets.