کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9960584 | 1577545 | 2005 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Resistance to clopidogrel: A review of the evidence
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کلمات کلیدی
ACSSATADPPCIVASPPGE1CYP450cAMP - cAMPGPIIb/IIIa - GPIIb / IIIaadenosine diphosphate - آدنوزین دی فسفاتCyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicSubacute stent thrombosis - ترومبوز استنت پس از قاعدگیacute coronary syndromes - سندرم های کرونری حادCytochrome P450 - سیتوکروم پی۴۵۰Vasodilator-stimulated phosphoprotein - فسفوپروتئین تحریک شده با واسوادولاتورpercutaneous coronary intervention - مداخله کرونری از راه پوستProstaglandin E1 - پروستاگلاندین E1glycoprotein IIb/IIIa - گلیکوپروتئین IIb / IIIa
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Resistance to clopidogrel: A review of the evidence Resistance to clopidogrel: A review of the evidence](/preview/png/9960584.png)
چکیده انگلیسی
Current available data show that about 4% to 30% of patients treated with conventional doses of clopidogrel do not display adequate antiplatelet response. Clopidogrel resistance is a widely used term that remains to be clearly defined. So far, it has been used to reflect failure of clopidogrel to achieve its antiaggregatory effect. The interpatient variability in clopidogrel response is multifactorial. It can be due to extrinsic or intrinsic mechanisms. Among extrinsic mechanisms are the possibility of clopidogrel underdosing in patients undergoing stenting or with acute coronary syndrome, and drug-drug interactions involving CYP3A4. Intrinsic mechanisms include genetic polymorphisms of the P2Y12receptor and of the CYP3As, accrued release of adenosine diphosphate, or up-regulation of other platelet activation pathways. Presently, there is no definite demonstration of an association between low responsiveness to clopidogrel and thrombotic events. The optimal level of clopidogrel-induced platelet inhibition, which will correlate quantitatively with clopidogrel's ability to prevent atherothrombotic events is still lacking. Furthermore, because there is no single and validated platelet function assay to measure clopidogrel's antiplatelet effect, it is not justified to routinely look for clopidogrel resistance in the clinical setting. This review discusses currently available evidence surrounding the variability in the antiplatelet response to clopidogrel.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the American College of Cardiology - Volume 45, Issue 8, 19 April 2005, Pages 1157-1164
Journal: Journal of the American College of Cardiology - Volume 45, Issue 8, 19 April 2005, Pages 1157-1164
نویسندگان
Thuy Anh MSc, Pharm, Jean G. MD, Chantal PharmD,