Aspirin Resistance in Trinidad.

Aspirin's beneficial effect is mediated via the inhibition of arachidonic acid (AA) activation of platelets. It is detected by demonstrating a decrease in platelet function and/or a decrease in prostaglandin metabolites. Besides inhibiting the formation of thromboxane A2 from arachidonic acid, Aspirin has a host of platelet-independent effects that complement its platelet-inhibitory effects. The phenomenon of "Aspirin resistance" is based on the observation of clinical events in some patients taking Aspirin and/or a diminished platelet aggregation inhibitory response to Aspirin therapy. It has been suggested that many individuals taking Aspirin have become resistant to this drug. Unfortunately, laboratory assays used to monitor the efficacy of Aspirin are far from accurate, and the results are not reproducible. Multiple studies demonstrate non-compliance using repeat testing for platelet inhibition in patients with an initial inadequate response to Aspirin. When the test is repeated under the condition that the ingestion of the test Aspirin is assured, the patients' platelets are inhibited. Patients with an inadequate Aspirin response have an increased likelihood of subsequent vascular events.