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Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease
OBJECTIVE: Laboratory tests including optical platelet aggregometry (OPA), platelet function analyser (PFA-100), and thromboxane B(2) (TXB(2)) metabolite levels have been used to define aspirin resistance. This study characterised the prevalence of aspirin resistance in patients with ischaemic heart...
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Formato: | Texto |
Lenguaje: | English |
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BMJ Publishing Group
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705011/ https://www.ncbi.nlm.nih.gov/pubmed/18697805 http://dx.doi.org/10.1136/hrt.2008.150631 |
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author | Muir, A R McMullin, M F Patterson, C McKeown, P P |
author_facet | Muir, A R McMullin, M F Patterson, C McKeown, P P |
author_sort | Muir, A R |
collection | PubMed |
description | OBJECTIVE: Laboratory tests including optical platelet aggregometry (OPA), platelet function analyser (PFA-100), and thromboxane B(2) (TXB(2)) metabolite levels have been used to define aspirin resistance. This study characterised the prevalence of aspirin resistance in patients with ischaemic heart disease (IHD) and investigated the concordance and repeatability of these tests. DESIGN, SETTING AND PATIENTS: Consecutive outpatients with stable IHD were enrolled. They were commenced on 150 mg aspirin daily (day 0) and had platelet function assessment (OPA and PFA-100) and quantitative analysis of serum/urine TXB(2) at day ⩾7 and then at a second visit approximately 2 weeks later. MAIN OUTCOME MEASURES: We assessed the prevalence of aspirin resistance by each method, concordance between methods of measuring response to aspirin and association between time points to assess the predictability of response over time. RESULTS: 172 patients (62.7 (SD 8.7) years, 83.1% male) were recruited. At visits 1 and 2, respectively, 1.7% and 4.7% were aspirin resistant by OPA, whereas 22.1% and 20.3% were aspirin resistant by PFA-100. There were poor associations between PFA-100 and OPA, and between TXB(2) metabolites and platelet function tests. OPA and PFA-100 results were poorly associated between visits (κ = 0.16 and κ = 0.42, respectively) as were TXB(2) metabolites, suggesting that aspirin resistance is not predictable over time. CONCLUSIONS: The prevalence of aspirin resistance is dependent on the method of testing. Response varies on a temporal basis, indicating that testing on a single occasion is inadequate to diagnose resistance or guide therapy in a clinical setting. |
format | Text |
id | pubmed-2705011 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-27050112009-08-12 Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease Muir, A R McMullin, M F Patterson, C McKeown, P P Heart Secondary prevention of coronary disease OBJECTIVE: Laboratory tests including optical platelet aggregometry (OPA), platelet function analyser (PFA-100), and thromboxane B(2) (TXB(2)) metabolite levels have been used to define aspirin resistance. This study characterised the prevalence of aspirin resistance in patients with ischaemic heart disease (IHD) and investigated the concordance and repeatability of these tests. DESIGN, SETTING AND PATIENTS: Consecutive outpatients with stable IHD were enrolled. They were commenced on 150 mg aspirin daily (day 0) and had platelet function assessment (OPA and PFA-100) and quantitative analysis of serum/urine TXB(2) at day ⩾7 and then at a second visit approximately 2 weeks later. MAIN OUTCOME MEASURES: We assessed the prevalence of aspirin resistance by each method, concordance between methods of measuring response to aspirin and association between time points to assess the predictability of response over time. RESULTS: 172 patients (62.7 (SD 8.7) years, 83.1% male) were recruited. At visits 1 and 2, respectively, 1.7% and 4.7% were aspirin resistant by OPA, whereas 22.1% and 20.3% were aspirin resistant by PFA-100. There were poor associations between PFA-100 and OPA, and between TXB(2) metabolites and platelet function tests. OPA and PFA-100 results were poorly associated between visits (κ = 0.16 and κ = 0.42, respectively) as were TXB(2) metabolites, suggesting that aspirin resistance is not predictable over time. CONCLUSIONS: The prevalence of aspirin resistance is dependent on the method of testing. Response varies on a temporal basis, indicating that testing on a single occasion is inadequate to diagnose resistance or guide therapy in a clinical setting. BMJ Publishing Group 2009-08-01 2009-08-12 /pmc/articles/PMC2705011/ /pubmed/18697805 http://dx.doi.org/10.1136/hrt.2008.150631 Text en © Muir et al 2009 http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Secondary prevention of coronary disease Muir, A R McMullin, M F Patterson, C McKeown, P P Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title | Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title_full | Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title_fullStr | Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title_full_unstemmed | Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title_short | Assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
title_sort | assessment of aspirin resistance varies on a temporal basis in patients with ischaemic heart disease |
topic | Secondary prevention of coronary disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705011/ https://www.ncbi.nlm.nih.gov/pubmed/18697805 http://dx.doi.org/10.1136/hrt.2008.150631 |
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