Development of aspirin resistance in persons with previous ischemic stroke.

Helgason, Cathy M.; Bolin, Kim M.; Hoff, J.; Winkler, Susan R.; Mangat, Amrit; Tortorice, Kathryn L.; Brace, Larry D.

doi:10.1161/01.str.25.12.2331

Cited by 375 publications

(251 citation statements)

References 17 publications

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“…Two reports showed that the extent of inhibition of platelet aggregation by aspirin progressively decreased over time in some patients, suggesting that some kind of aspirin tolerance may develop during chronic aspirin treatment. 50,75 This issue is controversial, because another study showed that 100 patients on chronic aspirin treatment had consistently reduced platelet aggregation over time. 76 …”

Section: Unproven Aspirin Resistancementioning

confidence: 99%

Aspirin and Clopidogrel

Cattaneo

2004

ATVB

371

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: Unproven Aspirin Resistancementioning

confidence: 99%

Aspirin and Clopidogrel

Cattaneo

2004

ATVB

371

133

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“…It is unclear if these observations reflect absorption problems or altered pharmacodynamics. 27,34 Aspirin in hypertensive patients: clinical implications and future research Coronary artery and cerebro-vascular diseases are the most common serious complications of long standing hypertension. The widespread use of aspirin probably contributes significantly to reduction of cardiovascular morbidity and mortality among high risk hypertensive patients with concomitant cardiovascular problems 35 and therefore there is a great potential for combined treatment with aspirin and ACE-I.…”

Section: Ace-i Induced Cough As a Clinical Marker Of Ace-i Activitymentioning

confidence: 99%

Clinical evidence of dose-dependent interaction between aspirin and angiotensin-converting enzyme inhibitors

et al. 2002

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Since coronary artery and cerebrovascular diseases are the most common serious complications of long standing hypertension, there is a great potential for combining treatment with aspirin and angiotensin-converting enzyme inhibitors (ACE-I). However, the data regarding interaction of aspirin and ACE-I in relation to blood pressure control and survival benefits are controversial and inconclusive. We presumed that the appearance of dry cough in some of the patients following initiation of ACE-I treatment could be used as a marker for the presence of their influence, whereas ACE-I cough attenuation after addition of aspirin to treatment could be a sign of aspirin and ACE-I interaction on clinical level. The present study was aimed to use ACE-I induced cough as a clinical marker of ACE-I activity to determine whether dose-dependent aspirin and ACE-I interaction does exist. In a cohort of 750 consecutive ACE-I treated hypertensive and postinfarction outpatients we identified 78 (10.4%) non-smoking ACE-I related coughers. Out of them, 31 (21 men, 10 women; mean age 61 ± 0.9 years) agreed to take part in the study, which was aimed to compare two regimens of combined ACE-I and aspirin treatment (self-matched control data): intermediate (500 mg daily) vs low-dose aspirin (100 mg daily). On each visit the life quality, cough severity (CS, 0-4) and frequency (CF, 0-10) scores were registered. Low doses

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“…Despite its large use, there are concerns about the efficacy of aspirin and methods to evaluate it [2,3]. Indeed, it appears that the antiplatelet effect of aspirin is not uniform in all patients and previous studies estimated that 8-45% of the population were aspirin resistant [4][5][6][7][8]. Most studies have focused on patients with coronary artery disease, although a few reports have identified aspirin resistance in patients with stroke or cerebrovascular disease [6][7][8][9].…”

Section: )1mentioning

confidence: 99%

“…Typically blood group O is associated with lower plasma VWF levels compared with non-O blood groups [4]. Non-O blood groups have also been shown to be associated with a higher incidence of CAD [5], which could in turn be determined by higher circulating VWF levels [7]. Inflammatory cytokines such as interleukin-1 and tumor necrosis factor-a [8] as well as procoagulant factors such as thrombin can influence the release of VWF from ECs [9].…”

Section: )1mentioning

confidence: 99%

Aspirin resistance in vitro and hypertension in stroke patients

Macchi¹,

Petit

Brizard³

et al. 2004

Journal of Thrombosis and Haemostasis

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France (mean ± SEM: 1.68 ± 0.03 vs. 1.58 ± 0.03 mg L )1 ; P ¼ 0.01). This difference appeared stronger in controls than in cases (Table 1), even though the interaction did not reach significance (P ¼ 0.38).As two studies have suggested a threshold effect in which low levels of protein Z increased the risk of thrombosis [4,6], we have stratified the population into two groups according to the 10th percentile of the distribution in controls. In the whole cohort, 10 percent (n ¼ 58) of healthy controls had protein Z levels below 0.93 mg L )1 (10th percentile ¼ 0.93 mg L )1). Eleven percent (n ¼ 32) of the patients had protein Z levels below this cut-off (P ¼ 0.58), which means that protein Z below 0.93 mg L )1 was not a risk factor for coronary disease.This was homogeneous across countries as 12% (n ¼ 21) and 10% (n ¼ 12) of the patients, in France and Northern Ireland, respectively, had protein Z levels below the 10th percentile which was set in controls for each country separately (P ¼ 0.47 and 0.80 for case-control difference in France and Northern Ireland, respectively).In conclusion, antigenic protein Z levels do not seem to have a major effect on the risk of coronary heart disease in healthy men followed for 5 years.

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Development of aspirin resistance in persons with previous ischemic stroke.

Cited by 375 publications

References 17 publications

Aspirin and Clopidogrel

Aspirin and Clopidogrel

Clinical evidence of dose-dependent interaction between aspirin and angiotensin-converting enzyme inhibitors

Aspirin resistance in vitro and hypertension in stroke patients

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