Aspirin Resistance: Detection, Mechanisms and Clinical Implications

被引：3

作者：

Linden, Matthew D. ^{[1
,2
,3
,4
]}

Frelinger, A. L., III ^{[1
,2
]}

Przyklenk, Karin ^{[1
,3
,4
]}

Furman, Mark I. ^{[1
,5
]}

Michelson, Alan D. ^{[1
,2
]}

机构：

[1] Univ Massachusetts, Med Sch, Ctr Platelet Funct Studies, Worcester, MA 01605 USA

[2] Univ Massachusetts, Med Sch, Dept Pediat, Worcester, MA 01605 USA

[3] Univ Massachusetts, Med Sch, Dept Emergency Med, Worcester, MA 01605 USA

[4] Univ Massachusetts, Med Sch, Dept Anesthesiol, Worcester, MA 01605 USA

[5] Univ Massachusetts, Med Sch, Dept Med, Div Cardiovasc Med, Worcester, MA 01605 USA

来源：

CURRENT CARDIOLOGY REVIEWS | 2005年 / 1卷 / 03期

关键词：

Aspirin; aspirin resistance; thromboxane; cyclooxygenase; 1; polymorphisms; treatment failure; antiplatelet therapy;

D O I：

10.2174/157340305774574134

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Aspirin, the most widely used antiplatelet agent, irreversibly acetylates the enzyme cyclooxygenase 1 (COX-1), thereby inhibiting platelet thromboxane synthesis and subsequent platelet aggregation. Although aspirin has been demonstrated to reduce the odds of serious atherothrombotic events and death in high-risk patients by 25%, subsets of patients fail to respond to therapy and continue to suffer atherothrombotic events. This aspirin treatment failure may be due to sub-optimal bioavailability (e.g. because of non-compliance or under-dosing) or may be a consequence of the as yet poorly understood phenomenon of aspirin resistance. In this review, we summarize the current laboratory methods used to identify aspirin-resistant patients, outline the cellular mechanisms that may contribute to aspirin resistance, and discuss the clinical implications of this important issue.

引用

页码：203 / 211

页数：9

共 92 条

[11] Cyclooxygenase COX-2a, a novel COX-2 mRNA variant, in platelets from patients after coronary artery bypass grafting [J].