Comparison of a rapid platelet function assay - Verify Now(TM) aspirin - with whole blood impedance aggregometry for the detection of aspirin resistance

Department of Medicine, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9073, United States.
Thrombosis Research (Impact Factor: 2.43). 02/2007; 120(4):485-8. DOI: 10.1016/j.thromres.2006.11.006
Source: PubMed
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    ABSTRACT: Objective: Assessment on platelet responsiveness to aspirin may be required in selected clinical conditions. So far, no standardization in laboratory practices for aspirin assessment using whole blood (WB) platelet aggregation based test. A study for method validation was performed to investigate the aspirin effects on platelets by comparing with a reference method. Methods: Forty patients taking aspirin were analyzed using WB by conventional platelet aggregometer (Chrono-Log Model 500CA/560CA). Among these patients, nine of them had their platelet rich plasma (PAP) tested by the same analyzer (reference method). Another WB specimens from 25 patients were tested on both Chrono-Log and Multiplate(R) (Dynabyte GmbH), which is a newer generation platelet function analyzer. Results: There were good and moderate agreements between WB on the Chronolog analyzer vs the reference method and WB on Chronolog vs WB on Multiplate(R) analyzers respectively. Conclusions: There are agreements between PRP and WB aggregation (WBA) methods in detecting aspirin effects on platelets. It is recommended that the test validation for the assessment of platelet responsiveness to aspirin is interpreted and correlated with the reference method preferably PAP.
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    ABSTRACT: High level of C-reactive protein (CRP), most popular inflammatory marker, increases the risk of thrombotic cardiovascular events. Aspirin, which has both anti-inflammatory and anti-thrombotic effects, has the potential to influence CRP release. Several studies have been reported investigating clinical effects of aspirin on CRP levels. Some studies have reported aspirin reduced CRP levels, but other studies did not. This study was designed to assess the effect of low-dose aspirin on CRP levels in controlled hypertensive patients who had low inflammatory burden. Two hundred twenty-five patients with controlled hypertension were randomly divided into two groups; aspirin group (n = 122, 100 mg of aspirin) and the control group (n = 134). Patients with a CRP level >1 mg/dL (10 mg/L) were excluded because these high levels suggest infection. C-reactive protein level and lipid profiles were measured before therapy and 3 months after therapy. There were no differences in baseline clinical characteristics between the two groups. Low-dose aspirin showed no significant influence on CRP levels over 3 months (from 0.10 ± 0.0099 to 0.12 ± 0.0097 mg/dL, p = 0.12). Statin therapy did not influence CRP levels. Aspirin-resistance also had no influence on CRP levels. We conclude that low-dose aspirin has no significant effect on decreasing CRP levels in the patients with controlled hypertension which had low inflammatory burden. The anti-inflammatory mechanism may not play an important role in the cardioprotective effect of aspirin in the population with low inflammatory burden such as controlled hypertensive patients.
    Clinical and Experimental Hypertension 02/2011; 33(1):47-52. DOI:10.3109/10641963.2010.503302 · 1.46 Impact Factor
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    ABSTRACT: Concerns have been raised about the potential adverse interaction between clopidogrel and PPIs. We studied the impact of esomeprazole and ranitidine on the antiplatelet action of clopidogrel and aspirin and sought to determine whether doubling the dose of clopidogrel could restore its efficacy. In a randomized prospective crossover study, we tested platelet reactivity to aspirin and clopidogrel (75 and 150 mg) with and without esomeprazole or ranitidine using the VerifyNow system (Accumetrics Inc, San Diego, CA, USA) in 4 stages, each lasting 7 days: T1, 160 mg aspirin and 75 mg clopidogrel; T2 : 160 mg aspirin+75 mg clopidogrel+20 mg esomeprazole, T3 : 160 mg aspirin+150 mg clopidogrel+20 mg esomeprazole and T4 : 160 mg aspirin+75 mg clopidogrel+150 mg ranitidine. Results are expressed in P2Y12 Reaction Units (PRU%) and Aspirin Reaction Units (ARU). In 21 patients with stable coronary artery disease, esomeprazole reduced the effect of clopidogrel with a 38.6%±24 loss in PRU% (p<0.001) (absolute mean difference -16.7 PRU% [-21;-12.5]), increasing 8-fold the prevalence of low responders to clopidogrel (defined as patients with PRU% below 20%). Doubling clopidogrel dosage to 150 mg restored the basal response. Ranitidine did not modify the antiplatelet effect of clopidogrel. Our study demonstrates a strong negative clopidogrel/esomeprazole interaction, compensated by increasing the dose of clopidogrel to 150 mg or replacing esomeprazole with ranitidine. That could offer a simple solution to the PPI-induced clopidogrel resistance.
    Thrombosis Research 07/2011; 128(5):458-62. DOI:10.1016/j.thromres.2011.06.029 · 2.43 Impact Factor