Abstract
Background and Objectives: Aspirin (acetylsalicylic acid—ASA) is a first-line antiplatelet therapy provided to patients with coronary artery disease (CAD). However, it has been demonstrated that 20–30% of these patients are non-sensitive to their ASA therapy. ASA non-sensitivity is a phenomenon where low-dose ASA (81–325 mg) does not completely inhibit arachidonic-acid-induced platelet aggregation, putting patients at risk of adverse cardio-thrombotic events. Ticagrelor is a P2Y12 receptor inhibitor and alternative antiplatelet that has been approved to reduce the risk of stroke, myocardial infarction, and overall cardiovascular-related death. In this study, we aimed to identify ASA non-sensitive patients and evaluate if they would be sensitive to ticagrelor. Materials and Methods: For this pilot study, thirty-eight patients with CAD taking 81 mg ASA were recruited. Blood samples were collected from each patient and platelet rich plasma (PRP) from each sample was isolated. Light-transmission aggregometry (LTA) was used to determine baseline ASA sensitivity in each patient using 0.5 mg/mL arachidonic acid as a platelet agonist. Patients with ≥20% maximal platelet aggregation after activation were considered ASA non-sensitive. Fresh PRP samples from all patients were then spiked with a clinical dosage of ticagrelor (3 μM—approximately equivalent to a loading dose of 180 mg ticagrelor). Sensitivity was determined using LTA and 5 μM ADP as a platelet agonist. Patients with ≥46% maximal platelet aggregation were considered ticagrelor non-sensitive. Results: Of the 38 CAD patients taking 81 mg ASA, 32% (12/38) were non-sensitive to their 81 mg ASA therapy. All 38 of the recruited patients (100%) were sensitive to ticagrelor ex vivo. In conclusion, we were able to identify ASA non-sensitivity using LTA and determine that ASA non-sensitive patients were sensitive to ticagrelor. Conclusions: Our results suggest that ticagrelor is a promising alternative therapy for patients who are non-sensitive to ASA.
Highlights
Patients with atherosclerotic diseases such as coronary artery disease (CAD), are at a greater risk of adverse cardio-thrombotic events such as myocardial infarction, stroke, and ischemia [1,2,3,4,5].Acetylsalicylic acid (ASA), better known by its commercial name aspirin, is a common medication used to treat fever, pain, and inflammation
We used light-transmission aggregometry to determine whether CAD patients who are non-sensitive to ASA would respond to ticagrelor
We have demonstrated using Light-transmission aggregometry (LTA), that CAD patients who are ASA non-sensitive may benefit from treatment with ticagrelor, as 100% of the ASA non-sensitive patients were sensitive to ticagrelor
Summary
Patients with atherosclerotic diseases such as coronary artery disease (CAD), are at a greater risk of adverse cardio-thrombotic events such as myocardial infarction, stroke, and ischemia [1,2,3,4,5].Acetylsalicylic acid (ASA), better known by its commercial name aspirin, is a common medication used to treat fever, pain, and inflammation. Patients with atherosclerotic diseases such as coronary artery disease (CAD), are at a greater risk of adverse cardio-thrombotic events such as myocardial infarction, stroke, and ischemia [1,2,3,4,5]. The antiplatelet effects of ASA have been well studied, and it is a cornerstone of secondary prevention of adverse cardio-thrombotic events in atherosclerotic patients [6,7,8,9]. ASA non-sensitive, defined as the inability of low-dose ASA (81–325 mg) to completely inhibit arachidonic-acid-induced platelet aggregation [11,12,13,14,15,16,17]. ASA non-sensitivity is a phenomenon where low-dose ASA (81–325 mg) does not completely inhibit arachidonic-acid-induced platelet aggregation, putting patients at risk of adverse cardio-thrombotic events.
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