Why the study?
COX inhibitors increase the risk of coronary events even with acute usage, contrasting with aspirin's cardiovascular benefits and evidence that COX inhibition protects vascular function.
What are the mechanisms mediating elevated cardiovascular disease risk with the use of COX inhibitors?
What are the mechanisms mediating elevated cardiovascular disease risk with the use of COX inhibitors?
This review proposes a novel mechanism involving prostanoids and T cells to explain the elevated cardiovascular risk associated with NSAID use.
Hypothesis-generating for prostanoid-T cell mediation of NSAID cardiovascular risk; leaves open prospective mechanistic validation.
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.
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Khan et al. (2019) studied this question.
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