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.

Aspirin is a wonder drug used for over 100 years for its analgesic and antipyretic effects. It is an inexpensive, readily available medication that reduces the risk of subsequent vascular disease by about 25% in patients with known occlusive vascular disease. For the past three decades, it has increasingly been used to prevent primary and secondary cardiovascular events.

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.

The POINT pilot study introduced the preliminary observation that the estimated prevalence of HPR is considerably higher within the heterogeneous population in Trinidad at 50% compared with predominantly Caucasian studies. Furthermore, the HPR is significantly higher in South Asians (Indo-Trinidadians) (>60% of patients), which has severe clinical repercussions considering the cardiovascular disease pandemic. Clopidogrel may not be a satisfactory or optimal antiplatelet agent in this subgroup. Therefore, another more potent antiplatelet, such as ticagrelor, should be used instead.

Patients generally displayed a limited level of cardiovascular medication adherence, which is likely to translate into a higher rate of cardiovascular events with their potentially devastating sequelae.

We postulate that there is a high level of Aspirin resistance in Trinidad and Tobago.

Inclusion Criteria:

1. between 18 and 74 years of age,
2. healthy with no overt medical conditions,
3. not on any physician-prescribed medications or complementary/alternative therapies,

Exclusion Criteria:

1. presence of active internal bleeding or history of bleeding diathesis or clinical findings associated with an increased risk of bleeding,
2. history of ischemic or hemorrhagic stroke, transient ischemic attack, intracranial neoplasm, arteriovenous malformation, or aneurysm,
3. clinical and/or hemodynamic instability,
4. within 1 month of placement of a bare metal stent,
5. within 30 days of coronary artery bypass graft surgery or PCI without a stent placed,
6. planned coronary revascularization,
7. treatment with fibrin-specific fibrinolytic therapy <24 h or non-fibrin-specific fibrinolytic therapy <48 h,
8. use of an oral anticoagulation agent or international normalized ratio >1.5,
9. body weight <60 kg,
10. age >75 years,
11. hemoglobin <10 g/dL,
12. platelet count <100×106/μL,
13. creatinine >2 mg/dL,
14. hepatic enzymes >2.5 times the upper limit of normal,
15. pregnancy and/or lactation,
16. the patient is on any other antithrombotic therapies such as ticagrelor, dabigatran, rivaroxaban and apixaban

All genders are included.