Resistance to aspirin in vitro at rest and during exercise in patients with angiographically proven coronary artery disease

Christiaens, Luc; Macchi, Laurent; Herpin, D.; Coisne, D.; Duplantier, C.; Allal, J; Mauco, Gérard; Brizard, A.

doi:10.1016/s0049-3848(03)00008-2

Cited by 62 publications

(40 citation statements)

References 30 publications

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“…As a matter of fact, Chakroun et al recently showed that high plasma VWF levels are the main determinant of short PFA-100 closure time in patients with cardiovascular disease on aspirin treatment, 61 and Watala et al demonstrated that VWF interaction with GPIb and GPIIb/IIIa is the major determinant of PFA-100 closure time, whereas other platelet receptors and mechanisms leading to platelet aggregation are of minor significance. 63 These findings explain the relatively high prevalence of short PFA-100 closure time in patients on aspirin treatment for cardiovascular or cerebrovascular disease, 42,43,[57][58][59][60][61][62] because these patients tend to have higher than normal levels of plasma VWF. Therefore, because aspirin does not inhibit the major determinants of the PFA-100 closure time, it appears that the PFA-100 system is not an adequate method to measure platelet inhibition by aspirin.…”

Section: Failure Of Aspirin To Inhibit Platelet Function In Vivo or Imentioning

confidence: 99%

“…This could easily account for the high percentage of subjects with short closure time despite being on aspirin treatment. 42,43,[57][58][59][60][61][62] Because the PFA-100 system studies platelet function under flow conditions that are characterized by high shear, plasma VWF is a major determinant of closure time. As a matter of fact, Chakroun et al recently showed that high plasma VWF levels are the main determinant of short PFA-100 closure time in patients with cardiovascular disease on aspirin treatment, 61 and Watala et al demonstrated that VWF interaction with GPIb and GPIIb/IIIa is the major determinant of PFA-100 closure time, whereas other platelet receptors and mechanisms leading to platelet aggregation are of minor significance.…”

Section: Failure Of Aspirin To Inhibit Platelet Function In Vivo or Imentioning

confidence: 99%

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Aspirin and Clopidogrel

Cattaneo

2004

ATVB

368

133

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Abstract-Aspirin and the thienopyridines ticlopidine and clopidogrel are antiplatelet agents that display good antithrombotic activity. In the past few years, the concept of aspirin resistance has been largely emphasized in the medical literature, although its definition is still uncertain. I suggest that "aspirin-resistant" should be considered as a description for those individuals in whom aspirin fails to inhibit thromboxane A 2 production, irrespective of the results of unspecific tests of platelet function, such as the bleeding time, platelet aggregation, or the PFA-100 system. Less well known than aspirin resistance, but certainly better characterized, is the issue of "clopidogrel resistance," which is probably mostly caused by inefficient metabolism of the prodrug clopidogrel to its active metabolite. At present, aspirin and clopidogrel resistance should not be looked for in the clinical setting, because there is no definite demonstration of an association with clinical events conditioning cost-effective changes in patient management. Key Words: aspirin resistance Ⅲ clopidogrel resistance Ⅲ antiplatelet agents Ⅲ cardiovascular diseases Ⅲ cerebrovascular diseases A spirin and the thienopyridines ticlopidine and clopidogrel are inhibitors of platelet aggregation that display good antithrombotic activity. They are used in the prophylaxis of patients undergoing vascular grafting or percutaneous angioplasty, in the medical management of acute coronary syndromes, and in long-term prevention of cardiovascular and cerebrovascular events.Both aspirin and the thienopyridines selectively inhibit a single pathway of platelet activation: aspirin affects the arachidonate-thromboxane A 2 (TxA 2 ) pathway by irreversibly inhibiting cyclo-oxygenase-1 (COX-1) (Figure 1). 1 The thienopyridines affect the adenosine diphosphate (ADP) pathway, by irreversibly blocking the ADP receptor P2Y 12 ( Figure 1). 2 Despite their selective mechanism of action, which does not counteract the many alternative pathways for platelet activation, aspirin and thienopyridines display a good antithrombotic activity. This is explained by the fact that both the arachidonate-TxA 2 pathway and the ADP pathway contribute to the amplification of platelet activation and are essential for the full aggregation and secretion response of platelets to agonists. 2

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Section: Failure Of Aspirin To Inhibit Platelet Function In Vivo or Imentioning

confidence: 99%

Section: Failure Of Aspirin To Inhibit Platelet Function In Vivo or Imentioning

confidence: 99%

Aspirin and Clopidogrel

Cattaneo

2004

ATVB

368

133

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“…The incidence of aspirin resistance ranges between 8-45% depending on timing and technique of examination, time of the last aspirin intake, dose of aspirin, and heterogenecity of patient population. [23][24][25][26] Several proposals have been put forward to explain the aspirin resistance; 1) lack of accommodation with aspirin treatment, 27) 2) impaired adsorption, 28) 3) use of other nonsteoridal antiinflammatory drugs, 28) 4) increased thromboxane production especially resistant to aspirin, 22) 5) increased platelet activation and/or turnover, 29) and 6) genetic polymorphism. 30) Grotemeyer, et al 26) found that patients with elevated platelet reactivity despite aspirin are more likely to experience vascular death, MI, or a cerebrovascular accident.…”

Section: Discussionmentioning

confidence: 99%

Heart Rate Variability in Patients With Stable Coronary Artery Disease and Aspirin Resistance

Durmaz¹,

Keleş²,

Özdemir³

et al. 2008

Int. Heart J.

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SUMMARYAspirin resistance as defined by failure to effectively inhibit thromboxane synthesis is associated with a higher risk of recurrent myocardial ischemia and cardiovascular death. Heart rate variability (HRV) analysis has been extensively used to identify patients at risk for increased cardiac mortality. The aim of this study was to evaluate the association between HRV and aspirin resistance in patients with stable coronary artery disease (CAD).Sixty-nine (69) consecutive patients with stable CAD were included in this study. Of the 69 patients, 18 (26%) were aspirin nonresponders. When the aspirin responders were compared with the nonresponders, there was no significant difference between the groups with respect to most clinical parameters, major cardiovascular risk factors, medical treatments, and aspirin dosages. However, the patients with aspirin resistance had a higher previous myocardial infarction history and lower left ventricular ejection fraction. Moreover, mean platelet volume, CT/EPI, CT/ADP values, LF and LF/HF ratio were higher while HF, SDNN, SDANN, and RMSSD were lower in the nonresponder group than the responders. Regarding HRV parameters, CT/ADP time was negatively correlated with SDNN (r = -0.5, P = 0.02) and HF (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.6, P = 0.01) and LF/HF (r = 0.7, P = 0.001). Similarly, CT/EPI time was negatively correlated with SDNN (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.5, P = 0.02) and the LF/HF ratio (r = 0.5, P = 0.02). Regression analysis revealed that the only parameters affecting SDNN and LF/HF ratio were left ventricle ejection fraction and aspirin resistance.The heart rate variability decreased and sympathetic activity increased in the patients with aspirin resistance and stable CAD. This may contribute to a higher risk of recurrent myocardial ischemia and cardiovascular death in patients with aspirin resistance. (Int Heart J 2008; 49: 413-422)

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“…If the collagen/epinephrine closure time was less than 187 seconds with 2.1% analytical variance, it was interpreted as aspirin resistance or aspirin insensitivity. 26 Serum levels of Hs-CRP were measured with a rate nephelometric method (IMMAGE Immunochemistry System; Beckman Coulter Inc., Brea, CA). The measurement range in this method was 0.2 to 1440 mg/L, and the reference range was < 7.44 mg/L.…”

Section: Asa Resistancementioning

confidence: 99%

Relationship Between Endothelial Functions and Acetylsalicylic Acid Resistance in Newly Diagnosed Hypertensive Patients

Şahı̇n

Geyık

Oner

et al. 2012

Clinical Cardiology

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Background: We aimed to investigate the effects and dose dependency of aspirin on endothelial functions and prevalence of aspirin resistance in newly diagnosed hypertensive patients without previous drug therapy and development of cardiac complications. Hypothesis: Acetylsalicyclic acid improves endothelial function. Methods: Fifty-eight hypertensive patients and 61 healthy subjects in the control group were included in the study. Endothelial functions of the patient and control groups were evaluated with brachial artery examination. Patient and control groups were divided into 2 groups. A total of 100 mg and 300 mg of aspirin were given to the separate groups for 1 week. After 1 week, endothelial functions were reevaluated and aspirin resistance examined with a platelet function analyzer (PFA-100; Dade Behring, Marbourg, Germany). Results: Baseline flow-mediated dilatation (FMD) change percent in hypertensive patients was 9.8%, and it was significantly lower than in the control group (12%) (P < 0.001). Frequency of acetylsalicylic acid (ASA) resistance was 20% and 26% in control and hypertensive patient groups, respectively (P = not significant). ASA resistance was 28% and 24% in 100 mg and 300 mg in hypertensive patients, respectively (P = not significant). FMD change percent increased both in the control and hypertensive groups after ASA treatment from 12.4% to 13.3% and 9.8 % to 11.9 %, respectively. FMD percentage change was significantly increased in hypertensive patients irrespective of ASA resistance (P = 0.02, for ASA resistance [+]; P < 0.012, for ASA resistance [−]). Conclusions: Endothelial functions were impaired more in hypertensive patients compared to the control group. Endothelial functions were improved with all ASA doses in hypertensive patients irrespective of ASA resistance. IntroductionThe vascular endothelium regulates cardiovascular homeostasis and blood pressure (BP) through the release of nitric oxide (NO).1,2 NO is an anti-inflammatory, antithrombotic, and antiproliferative agent that limits expression of adhesion molecules and chemotactic factors on endothelium, and inhibits platelet aggregation and proliferation of smooth muscle cells.

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Resistance to aspirin in vitro at rest and during exercise in patients with angiographically proven coronary artery disease

Cited by 62 publications

References 30 publications

Aspirin and Clopidogrel

Aspirin and Clopidogrel

Heart Rate Variability in Patients With Stable Coronary Artery Disease and Aspirin Resistance

Relationship Between Endothelial Functions and Acetylsalicylic Acid Resistance in Newly Diagnosed Hypertensive Patients

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