No clinical study data is present in the provided text, which consists only of journal editorial board information.
Does arachidonic acid-induced platelet aggregation and thromboxane A2 generation differ between male survivors of myocardial infarction and healthy controls?
Platelets from male survivors of myocardial infarction demonstrate hyperreactivity to arachidonic acid and increased thromboxane A2 generation, suggesting a potential ex vivo marker to identify patients who may benefit from targeted antiplatelet therapy.
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 AA were 746 +/- 62 micrometer, and 869 +/- 57 micrometer, respectively. Only in 2 healthy subjects, but in 12 patients, irreversible platelet aggregation was induced consistently with low concentrations of AA, under 500 micrometer. 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.
Szczeklik et al. (Sun,) reported a other. No clinical study data is present in the provided text, which consists only of journal editorial board information.