2007
DOI: 10.1016/j.ijcard.2006.10.025
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The frequency of aspirin resistance and its risk factors in patients with metabolic syndrome

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Cited by 22 publications
(23 citation statements)
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References 38 publications
(40 reference statements)
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“…In the study by Goksel et al ., this trend is clearly seen. [4] Current available data shows that about 4-30% of patients treated with conventional doses of clopidogrel do not display adequate antiplatelet response. Intrinsic mechanisms include genetic polymorphisms of the P2Y 12 receptor and of the CYP3As, accrued release of adenosine diphosphate, or upregulation of other platelet activation pathways.…”
Section: Introductionmentioning
confidence: 99%
“…In the study by Goksel et al ., this trend is clearly seen. [4] Current available data shows that about 4-30% of patients treated with conventional doses of clopidogrel do not display adequate antiplatelet response. Intrinsic mechanisms include genetic polymorphisms of the P2Y 12 receptor and of the CYP3As, accrued release of adenosine diphosphate, or upregulation of other platelet activation pathways.…”
Section: Introductionmentioning
confidence: 99%
“…This has raised the possibility that these patients may be resistant to aspirin and generated much interest in identification of such patients with laboratory tests of platelet function. Although many studies have demonstrated aspirin resistance in cardiovascular disorders including coronary artery disease [8,9], metabolic syndrome [10], and diabetes [11][12][13] by certain tests of aspirin resistance, there are still concerns that these tests have not correlated closely with subsequent recurrent events, and have not reliably identified non-responders to antiplatelet therapy [14][15][16]. In addition to the absence of any standardized approach to the diagnosis, there is currently no proven effective treatment for aspirin resistance.…”
Section: Introductionmentioning
confidence: 99%
“…Previously, investigations have found that inhibition of the function of platelets by aspirin is diminished in metabolic syndrome. 32, 33, 40, 41 However, platelet function assays ( e.g., ADP- and collagen-induced aggregation, PFA-100 ® , and VerifyNow ® ) indirectly measure the net effects of both thromboxane-dependent and thromboxane-independent pathways. Although these tests may provide information about platelet reactivity, they cannot determine the success or failure of aspirin to inhibit platelet COX-1 in an individual patient.…”
Section: Discussionmentioning
confidence: 99%