期刊
PHARMACOLOGY & THERAPEUTICS
卷 217, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2020.107665
关键词
Opioid-P2Y(12) inhibitor interaction; Acute myocardial infarction; High on treatment platelet reactivity; Analgesia in chest pain; Pain relief in myocardial infarction; Opioid-antiplatelet drug interaction
资金
- National Heart foundation fellowship, Australia
- Monash University, Australia Graduate Excellence Scholarship
- RTP
The treatment of chest pain associated with acute myocardial infarction has remained relatively unchanged since the 1930s when opioids were first utilized. However, concerns have arisen regarding the delayed gastrointestinal absorption of P2Y(12) inhibitors due to opioids and the subsequent impairment in antiplatelet activity. With a lack of randomized clinical trial evidence to support widespread opioid use, there is now an opportunity to re-evaluate our approach to analgesia in myocardial infarction.
Despite advances in medical and interventional management of acute myocardial infarction, treatment of the associated chest pain has remained relatively unchanged since opioids were first utilized in the 1930's. This dominance can be partially attributed to initial studies suggesting hemodynamic benefits with opioid treatment. However, delayed gastrointestinal absorption of P2Y(12) inhibitors due to opioids and the consequent impairment in antiplatelet activity of this established therapy is cause for concern. Coupled with the lack of randomized clinical trial evidence to support widespread opioid use, there is now an opportunity to re-evaluate our approach to analgesia in myocardial infarction. This review characterizes the mechanism of the opioid-P2Y(12) inhibitor interaction, strategies aimed at mitigating the interaction and appraises promising alternative agents to opioid therapy in patients with myocardial infarction. (C) 2020 Elsevier Inc. All rights reserved.
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