Antiplatelet effect of once- or twice-daily aspirin dosage in stable coronary artery disease patients with diabetes.

The aim of this pilot study was to compare the effect of two different regimens of aspirin dosage on platelet of coronary artery disease (CAD) diabetic patients. Twenty-five CAD diabetic patients were included. Initially, all patients received aspirin 100 mg/day for 10 days. At day 10, aspirin antiplatelet effect was determined by measuring the collagen/epinephrine closure time (CT) 2 h after the last aspirin dosage and the next morning at 8 a.m.. The aspirin regimen was modified to 100 mg twice daily for patients showing a non-optimal platelet-inhibitory effect (CT < 298 s at 8 a.m.). Persistent high platelet reactivity (HPR) was defined by a CT < 160 s. During the 100 mg/day aspirin regimen, the prevalence of HPR at 8 a.m. was 48%, and only 7 patients (28%) had showed an optimal platelet-inhibitory effect. Bridging to the twice-daily regimen, the HPR was significantly reduced (p=0.025), and the optimal platelet-inhibitory effect was reached for 3 other patients. Our results showed that 100 mg aspirin twice-daily dosing rather than a once-daily dose significantly improves the aspirin effect on platelet of CAD diabetic patients. However, large prospective studies were needed to confirm whether this strategy will be clinically relevant and safe.

Response variability to aspirin and one-year prediction of vascular events in patients with stable coronary artery disease.

The aim of this study was to assess the association between "aspirin non responsiveness" in patients with coronary artery diseases (CAD) and the risk of major adverse cardiovascular events (MACE). 204 patients with CAD receiving aspirin (250 mg/d) were included. Both Collagen/Epinephrine Closure Time (CEPI-CT) and urinary Thromboxane B2 (uTxB2) concentration was used to determine the patients aspirin responsiveness. The clinical primary endpoint was the occurrence of MACE including: cardiovascular death, MI, stroke or transient ischemic attack. The secondary endpoint was the occurrence of Recurrent Acute Vascular Event (RAVE: MI, stroke or transient ischemic attack). After 1-year follow-up, no responders diagnosed by CEPI-CT had a trend for higher risk of MACE (13% vs 7.4%; P = 0.22) and significant higher risk of RAVE (OR = 2.1; 95%CI: 1.7-2.4; P = 0.01) when compared to good responders. Multivariate analysis showed that CEPI-CT < 143 s was the only independent predictor of RAVE (OR = 6.3; 95% CI: 1.2-32.2; P = 0.026). Aspirin non-responsiveness, diagnosed by the uTxB2, was not associated with an increased risk of either MACE or RAVE. Our results, reinforce the importance of being able to diagnose laboratory "aspirin non responsiveness", and extend the evidence that aspirin non responsiveness may explain in part the occurrence of RAVE.

Screening for aspirin resistance in stable coronary artery patients by three different tests.

BACKGROUND: Aspirin (ASA) failure to inhibit in vitro platelet function had been termed ASA resistance. The prevalence of this phenomenon as measured with different platelet function tests varies widely among studies. OBJECTIVES: In this study, we propose to determine the prevalence of ASA non-responsiveness in stable coronary artery patients using three different tests. PATIENTS AND METHODS: One hundred ninety-one patients with a stable coronary artery disease and receiving secondary ASA prophylaxis (250 mg/day) were tested. For each patient the ASA-induced platelet inhibition was determined using three different tests: Ivy Bleeding time (BT), collagen/epinephrine closure time (CEPI-CT; PFA-100, Dade-Behring) and urinary 11-dehydrothromboxane B2 (uTxB2) excretion level. The agreement between these tests was evaluated by kappa statistics test. RESULTS: The prevalence of biological ASA resistance was 15.7% (n=30), 20.4% (n=39) and 24.6% (n=47) by BT, PFA-100 and UTxB2, respectively. Only fourteen patients (7.3%) were non-responders for two tests: 6 (3.1%) BT/ PFA-100; 1 (0.5%) BT/UTxB2; 7 (3.7%) PFA-100/UTxB2). A poor agreement was found between these three methods and only 3 patients were resistant with all the tests (1.6%). CONCLUSION: The lack of agreement supposed that different types of aspirin resistance exist. Thus, combination of two tests or more could be a primary solution for a better identification of ASA resistant patients. This hypothesis must be confirmed by a large-scale randomized study with clinically well-defined endpoints.