No abstract

Several studies indicate that a biochemically reduced response to aspirin increases the risk of cardiovascular events. This study was designed to investigate the performance of Multiplate whole blood aggregometry as regards assessment of platelet function prior to and after aspirin treatment, and to compare it with light transmission aggregometry (LTA). We included 21 healthy individuals and 43 patients with documented coronary artery disease (CAD). Platelet aggregation induced by arachidonic acid 0.5 mM was measured in duplicate by Multiplate aggregometry and LTA in healthy individuals before aspirin treatment and in all participants on four consecutive days during treatment with 75 mg aspirin daily. Optimal compliance was confirmed by complete suppression of serum thromboxane B(2) in all participants. Employing the Multiplate, the coefficient of variation (CV) was lower at baseline (CV = 8%) than during aspirin treatment in both healthy individuals (CV = 46%) and patients (CV = 46%). During aspirin treatment, the repeatability of LTA was superior to Multiplate measurements. However, the Multiplate was superior to LTA as regards the ability to discriminate platelet response before and after aspirin treatment. In conclusion, the repeatability of Multiplate aggregometry was good before aspirin treatment, whereas the CV was quite high during aspirin treatment in both healthy individuals and patients. However, the Multiplate device was fully capable of assessing platelet function prior to and after treatment with aspirin. Clinical studies are needed to investigate whether a high platelet aggregation level measured by Multiplate whole blood aggregometry during aspirin treatment is associated with a poor clinical outcome.

Individualised antiplatelet therapy and platelet function testing have attracted considerable clinical interest, but several aspects of test performance have not been thoroughly evaluated. We investigated repeatability and concordance of light transmission aggregometry (LTA) induced with arachidonic acid (AA) 1.0 mM, PFA-100 induced with collagen/epinephrine, multiple electrode aggregometry (MEA) induced with AA 0.5 or 0.75 mM and VerifyNow Aspirin. Patients with stable coronary artery disease (n=43) and healthy individuals (n=21) were included. All tests were performed in duplicate at baseline in healthy individuals and in duplicate for four days in all study participants during aspirin treatment. Serum and urinary thromboxane metabolites were measured several times to evaluate cyclooxygenase-1 inhibition by aspirin. MEA was most sensitive for aspirin as treatment induced a 12-fold difference in AA-induced platelet aggregation. Coefficients of variation for duplicate measurements at baseline (0.4-12%), during aspirin treatment (3-46%) and for day-to-day variability (3-37%) differed markedly between tests and were lowest for VerifyNow. The prevalence of aspirin low-responsiveness also differed between tests (0-9%) and the agreement was low: kappa

No abstract

Objective: Randomized clinical trials have reported low risks of bleeding in non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients receiving triple antithrombotic treatment (aspirin, clopidogrel and heparin). As trial patients often differ substantially from unselected patients treated in routine clinical settings, we compared the incidence of bleeding in ‘real-life patients’ with the incidence in the CURE (Clopidogrel in Unstable Angina to Prevent Recurrent Events) trial. Methods: We conducted a historical follow-up study based on 195 nonselected patients diagnosed with NSTE-ACS admitted to a Danish hospital. Data were obtained through systematic review of medical records. Bleeding complications were registered for 6 months after the event. Results: One hundred and nineteen (61.0%) patients fulfilled the inclusion and exclusion criteria of the CURE trial and were treated with triple antithrombotic therapy. Eleven (9.2%) of the 119 patients suffered a life-threatening bleeding. Their relative risk of life-threatening bleeding was 4.3 (95% CI 2.4–7.7) compared with the CURE study population. There was no difference in minor bleeding. Among patients not eligible according to the CURE criteria, but receiving intensive antithrombotic treatment, the relative risk of life-threatening bleeding was 6.4 (95% CI 3.1–12.9). Conclusions: When triple antithrombotic therapy is used in clinical practice in NSTE-ACS patients, the risk of bleeding may exceed that reported in trials. Assessment of the bleeding risk in the individual patient is warranted.