Prevalence and biologic profile of aspirin resistance in patients with angiographically proven coronary artery disease

Narvaez, I.; Sagastagoitia, José Domingo; Vacas, Marta; Sáez, Yolanda; Lafita, Manolo; Santos, Mónica; Lafuente, Jesús Pablo Sáez de; Molinero, E; Iriarte, J.A.

doi:10.1016/j.thromres.2006.12.020

Cited by 17 publications

(10 citation statements)

References 36 publications

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“…A similar finding was reported by Narvaez et al when resistance to aspirin was defined by PFA-100 ® results [22]. The relation of TxA 2 formation to platelet aggregation is not linear and near complete inhibition of TxA 2 synthesis by aspirin is required to achieve sustained inhibition of platelet function [23][24][25].…”

Section: Discussionsupporting

confidence: 68%

Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin

Lordkipanidzé

Diodati

Turgeon

et al. 2010

International Journal of Cardiology

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Section: Discussionsupporting

confidence: 68%

Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin

Lordkipanidzé

Diodati

Turgeon

et al. 2010

International Journal of Cardiology

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“…Extending these results, the present study showed that platelet aggregation evaluated by VerifyNow is also dependent on platelet count, even within the normal range of platelet count. In studies performing platelet aggregation analyses using light transmission aggregometry [ 17 ] or the Platelet Function Analyzer-100 [ 18 ], an association between platelet count and platelet aggregation in stable CAD patients has also been reported.…”

Section: Discussionmentioning

confidence: 99%

Determinants of Reduced Antiplatelet Effect of Aspirin in Patients with Stable Coronary Artery Disease

et al. 2015

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BackgroundAspirin is a cornerstone in management of coronary artery disease (CAD). However, considerable variability in the antiplatelet effect of aspirin has been reported.AimTo investigate independent determinants of reduced antiplatelet effect of aspirin in stable CAD patients.MethodsWe performed a cross-sectional study including 900 stable, high-risk CAD patients. Among these, 795 (88%) had prior myocardial infarction, 250 (28%) had type 2 diabetes, and 170 (19%) had both. All patients received 75 mg aspirin daily as mono antiplatelet therapy. The antiplatelet effect of aspirin was assessed by measurement of platelet aggregation employing 1) multiple electrode aggregometry (MEA, Multiplate Analyzer) in whole blood anticoagulated with citrate or hirudin using arachidonic acid (AA) or collagen as agonists, and 2) VerifyNow Aspirin Assay. Compliance was assessed by measurement of serum thromboxane B2.ResultsPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased AA-induced MEA platelet aggregation in citrate and hirudin anticoagulated blood (p-values ≤ 0.045). Similar results were found with VerifyNow. Prior coronary artery bypass grafting, age, smoking (MEA, AA/citrate) and female gender (MEA, AA/hirudin) were also independent determinants of increased platelet aggregation (p-values ≤ 0.038). Compliance was confirmed by low serum thromboxane B2 levels in all patients (median [25%;75%]: 0.97 [0.52;1.97], range 0.02-26.44 ng/ml).ConclusionPlatelet count, prior myocardial infarction, type 2 diabetes and body mass index were independent determinants of increased platelet aggregation, indicating that these characteristics may be key factors in reduced antiplatelet effect of aspirin in stable CAD patients.

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“…Similar to our data, Wang and coworkers 41 found that platelet count was a statistically significant univariate and multivariate predictor of aspirin nonresponsiveness when treated as continuous variables, with OR of 0.993. However, Lee and coworkers 42 and Navaez and coworkers 43 found that high platelet count was related with aspirin resistance. We believe that these conflicting results might be due to the multifactorial nature of aspirin resistance.…”

Section: Discussionmentioning

confidence: 99%

Aspirin Resistance in Hypertensive Patients

Özben¹,

Tanrikulu²,

Özben³

et al. 2010

J of Clinical Hypertension

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J Clin Hypertens (Greenwich). 2010;12:714–720. ©2010 Wiley Periodicals, Inc. Aspirin resistance is associated with poor clinical prognosis. The authors investigated aspirin resistance in 200 hypertensive patients (111 men, age: 68.3±11.4 years) by the Ultegra Rapid Platelet Function Assay‐ASA (Accumetrics Inc., San Diego, CA). Aspirin resistance was defined as an aspirin reaction unit ≥550. Aspirin resistance was detected in 42 patients. Aspirin resistance was present in 25.6% of the patients with poor blood pressure control, while in 17.8% of the patients with controlled blood pressure (P=.182). Female gender and creatinine levels were significantly higher (P=.028 and P=.030, respectively), while platelet count was significantly lower (P=.007) in aspirin‐resistant patients. Multivariate analysis revealed that female gender (odds ratio [OR], 2.445; P=.045), creatinine levels (OR, 1.297; P=.015) and platelet count (OR, 0.993; P=.005) were independent predictors of aspirin resistance. The frequency of aspirin resistance is not low in hypertensive patients. Female hypertensive patients, especially, with higher creatinine levels and lower platelet count are at higher risk for aspirin resistance.

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Prevalence and biologic profile of aspirin resistance in patients with angiographically proven coronary artery disease

Cited by 17 publications

References 36 publications

Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin

Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin

Determinants of Reduced Antiplatelet Effect of Aspirin in Patients with Stable Coronary Artery Disease

Aspirin Resistance in Hypertensive Patients

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