Department of Pharmacology, Monash University, Clayton, Victoria 3800, Australia.
Baker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia.
Int J Mol Sci. 2019 Aug 30;20(17):4262. doi: 10.3390/ijms20174262.
Cyclo-oxygenase (COX) inhibitors are among the most commonly used drugs in the western world for their anti-inflammatory and analgesic effects. However, they are also well-known to increase the risk of coronary events. This area is of renewed significance given alarming new evidence suggesting this effect can occur even with acute usage. This contrasts with the well-established usage of aspirin as a mainstay for cardiovascular prophylaxis, as well as overwhelming evidence that COX inhibition induces vasodilation and is protective for vascular function. Here, we present an updated review of the preclinical and clinical literature regarding the cardiotoxicity of COX inhibitors. While studies to date have focussed on the role of COX in influencing renal and vascular function, we suggest an interaction between prostanoids and T cells may be a novel factor, mediating elevated cardiovascular disease risk with NSAID use.
环氧化酶 (COX) 抑制剂因其抗炎和镇痛作用而成为西方世界最常用的药物之一。然而，它们也因增加冠状动脉事件的风险而广为人知。鉴于令人震惊的新证据表明，即使是急性使用也可能发生这种作用，这一领域重新引起了关注。这与阿司匹林作为心血管预防的主要药物的既定用途形成鲜明对比，而且有压倒性的证据表明 COX 抑制诱导血管扩张，对血管功能具有保护作用。在这里，我们对 COX 抑制剂的心脏毒性的临床前和临床文献进行了更新回顾。虽然迄今为止的研究集中在 COX 对影响肾脏和血管功能的作用上，但我们认为前列腺素和 T 细胞之间的相互作用可能是一个新的因素，介导 NSAID 使用时心血管疾病风险的升高。
