Abstract
Introduction. Laboratory tests do not reveal any changes due to administration of aspirin (75 – 150 mg/d) in about 25% of patients. The definition of aspirin resistance and parameters of different laboratory tests for its identification have not yet been established.
Aim. The aim of our study was to compare the results of platelet aggregation studies, the closure times in PFA-100, the plasma concentrations of 11-dehydro thromboxane B2 (11-d TxB2) and 8-epi prostaglandin F2α (8-epi PgF2α) in patients receiving aspirin chronically.
Material. The study group consisted of 22 patients taking aspirin for the secondary prevention of ischemic stroke (IS). All patients were at least 6 months after the acute onset, and had a diminished intraplatelet concentration of malonyldialdehyde due to aspirin ingestion.
Methods. Following parameters have been evaluated:
Platelet aggregation induced by either ADP (3,5 and 5,0 μM), collagen (2 μg/ml) or arachidonic acid (AA) (0,6 mM);
Closure time in PFA-100 (collagen/epinephrine and collagen/ADP cartridges);
Plasma 11-d TxB2 and 8-epi PgF2α concentration measured by ELISA method (Cayman Chemicals).
Aspirin resistance has been determined by the following criteria: the intensity of ADP induced platelet aggregation ≥ 60%, collagen induced aggregation ≥ 70%, AA induced aggregation ≥ 20%, PFA-100 closure time ≤ 165 s, 11-d TxB2 concentration ≥ mean of the control group ± 2 SD.
Results.
Aggregation . | . | . | |||
---|---|---|---|---|---|
ADP 3,5 μM . | ADP 5,0 μM . | Collagen . | Arachidonic acid . | PFA-100 . | 11-d TxB2 . |
63,6% | 45,5% | 18,2% | 13,6% | 54,5% | 50,0% |
Aggregation . | . | . | |||
---|---|---|---|---|---|
ADP 3,5 μM . | ADP 5,0 μM . | Collagen . | Arachidonic acid . | PFA-100 . | 11-d TxB2 . |
63,6% | 45,5% | 18,2% | 13,6% | 54,5% | 50,0% |
Statistically significant correlations have been found between the plasma concentration of 11-d TxB2 and PFA-100 (Col/Epi) closure times and between plasma concentration of 8-epi PgF2α and PFA-100 (Col/Epi) closure times. There was no difference in mean plasma concentration of 8-epi PgF2α between the group of patients and controls.
Conclusions.
The most valid laboratory method of aspirin resistance identification in ischemic stroke patients (besides a mesurement of 11-dehydro thromboxane B2) seems to be PFA-100 closure time.
Our PFA-100 studies reveal a much higher percentage of aspirin resistance as compared to former studies.
The plasma concentration of 8-epi prostaglandin F2α remains in the normal range in patients taking aspirin for the secondary prevention of ischemic stroke.
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