Aspirin resistance: position paper of the Working Group on Aspirin Resistance

Michelson, Allan D.; Cattaneo, Marco; Eikelboom, John W.; Gurbel, Paul A.; Kottke‐Marchant, K.; Kunicki, Thomas J.; Pulcinelli, Fabio M.; Cerletti, Chiara; Rao, A. Koneti

doi:10.1111/j.1538-7836.2005.01351.x

Cited by 306 publications

(227 citation statements)

References 7 publications

(23 reference statements)

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“…In conclusion, the present meta-analysis conducted in 11 prospective studies and including over than 1900 patients with CHD demonstrated that RPR is significantly associated with an increased risk of recurrent cardiovascular events, by possibly suggesting a clinical implication of RPR, though in apparent contrast with the indications of the scientific associations [27]. However, more prospective studies are needed to determine the independent prognostic importance of RPR during aspirin therapy and the possible benefit of individually tailored anti-platelet treatment strategies in these patients.…”

Section: Discussionmentioning

confidence: 61%

Residual platelet reactivity on aspirin therapy and recurrent cardiovascular events — A meta-analysis

Sofi

Marcucci

Gori

et al. 2008

International Journal of Cardiology

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Background: Recently, a growing body of evidence on the possible role of residual platelet reactivity (RPR) in affecting clinical events has accumulated. The aim of this study was to systematically assess the relationship between RPR on acetylic salicylic acid (ASA) therapy and the occurrence of recurrent events in a meta-analysis of prospective studies. Methods: A systematic literature search of MEDLINE, EMBASE, Science Citation Index, the Cochrane Systematic Review Database and bibliographies of retrieved articles through May 2007 was conducted. Studies were included if they analysed RPR in coronary heart disease patients in relation to the occurrence of adverse coronary events during follow-up. Results: Eleven prospective studies, incorporating 1952 patients with coronary heart disease followed for a time ranging from 6 days to 4 years, met the inclusion criteria. The pooled analysis demonstrated a significantly increased relative risk of adverse clinical events during follow-up for patients with RPR on ASA therapy (RR: 3.11, 95%CI 1.88-5.15; p b 0.0001). Moreover, the association between RPR and cardiovascular recurrences remained to be statistically significant even when subgroup analyses performed according to the duration of follow-up, ASA dosage, characteristics of the study population, and laboratory method were conducted. Conclusions: The present meta-analysis documents a significant association between RPR on ASA treatment and recurrent cardiovascular events. More prospective studies are needed to determine the independent prognostic importance of RPR during aspirin therapy and possible benefit of individually tailored anti-platelet treatment strategies in these patients.

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Section: Discussionmentioning

confidence: 61%

Residual platelet reactivity on aspirin therapy and recurrent cardiovascular events — A meta-analysis

Sofi

Marcucci

Gori

et al. 2008

International Journal of Cardiology

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“…In large secondary prevention trials, low-dose aspirin has been found to reduce the risk of stroke, myocardial infarction and cardiovascular death by 20% in high-risk patients 4,5) . However, a considerable number of patients continue to experience athero-thrombotic events despite receiving aspirin therapy 6,7) . Platelet reactivity during antiplatelet treatment can be assessed using various test systems 8) and exhibits great interindividual variability in all assays.…”

Section: Introductionmentioning

confidence: 99%

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Gremmel

Perkmann

Seidinger

et al. 2013

JAT

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Aims: Inflammation has been postulated to modify the platelet response to aspirin treatment, thereby causing high on-treatment residual platelet reactivity (HRPR). Both high levels of inflammatory markers and HRPR have been linked to adverse cardiovascular events. We aimed to study the impact of inflammation on residual arachidonic acid (AA)-inducible platelet reactivity. Methods: In 288 patients receiving dual antiplatelet therapy, residual AA-inducible platelet reactivity was assessed using light transmission aggregometry (LTA), the VerifyNow assay, multiple electrode aggregometry (MEA) and the Impact-R. The levels of urinary 11-dehydro-thromboxane B2 (D-TXB2), serum thromboxane B2 (TXB2), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were determined using immunoassays. Results: The IL-6 level was found to be an independent predictor of platelet reactivity as determined according to LTA and D-TXB2 using a multiple linear regression analysis. Accordingly, patients with supramedian IL-6 levels exhibited significantly higher platelet reactivity than patients with inframedian IL-6 levels when determined according to LTA and D-TXB2 (both p ≤ 0.02). High IL-6 levels were associated with a 3.6-fold (95%CI 2.1-6.4) increased risk of HRPR, as defined according to D-TXB2, and a 3.4-fold (95%CI 1.4-8.3) increased risk of HRPR, as defined according to MEA. The HsCRP level was found to be an independent predictor of platelet reactivity when determined according to LTA, D-TXB2, the Impact-R and TXB2 using a multiple linear regression analysis. High hsCRP levels were associated with a 3.6-fold (95%CI 1.3-10) increased risk of HRPR, as defined according to LTA, and a 2.5-fold (95%CI 1.3-4.6) increased risk of HRPR, as defined according to TXB2. Conclusions: Increased levels of inflammatory markers are independently associated with residual AA-inducible platelet reactivity in patients receiving dual antiplatelet treatment.

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“…This led to the suggestion that ASA might be ineffective in certain patients. Other investigators demonstrated that the anti-platelet properties of ASA can vary between individuals, and that recurrent events in some patients may be explained by residual platelet function due to "ASA resistance" or "non-responsiveness" [6,7].…”

Section: Introductionmentioning

confidence: 99%

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

et al. 2009

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Edelgard Lindhoff-Last. Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up. Annals of Hematology, Springer Verlag, 2009, 88 (10) Abstract Non-responsiveness to aspirin as detected by laboratory tests may identify patients at high risk for future vascular events. The aim of this prospective study was to evaluate whether non-responsiveness to aspirin is stable over time. Ninety-eight patients with stable peripheral arterial occlusive disease (PAOD) treated with 100 mg/d aspirin were followed over a median timeframe of 17 months. Platelet function tests were performed initially and at follow-up using arachidonic acid-induced light transmittance aggregometry (LTA) in native platelet-rich plasma with the Behring Coagulation Timer® and by measuring the collagen−epinephrine closure time (CT) on a Platelet Function Analyzer (PFA-100®). When determining platelet function using LTA, four patients (4.1%) had residual platelet function (i.e., MaxAggr ≥78%) despite aspirin treatment, whereas, according to the PFA-100® results, 12 patients (12.2%) were identified as nonresponders (i.e., CT <192 s). Fifty-seven patients who were still under treatment with 100 mg/d aspirin at the time of follow-up provided a second blood sample. Further platelet function tests with the PFA-100® system identified a persistent non-responsiveness to aspirin over time in three patients (5.3%) whereas four (7.0%) and 15 (26.3%) patients had changes in response status when platelet function was assessed by LTA and on the PFA-100®, respectively. We conclude that true non-responsiveness to aspirin is a rare phenomenon in stable PAOD patients.Furthermore, we conclude that in a number of patients, aspirin non-responsiveness is not stable over time.

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Aspirin resistance: position paper of the Working Group on Aspirin Resistance

Cited by 306 publications

References 7 publications

Residual platelet reactivity on aspirin therapy and recurrent cardiovascular events — A meta-analysis

Residual platelet reactivity on aspirin therapy and recurrent cardiovascular events — A meta-analysis

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Variability of non-response to aspirin in patients with peripheral arterial occlusive disease during long-term follow-up

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