Abstract
The prognosis after a myocardial infarction is now importantly linked to the reperfusion injury, which consists in cellular death due to reperfusion by itself. This ischemia/reperfusion phenomenon is mediated by the inflammatory response to myocardial infarction, mainly through the secretion of pro-inflammatory and anti-inflammatory cytokines by macrophages. Many treatments has been developed to target that inflammatory response, but the effects of standard treatments of the myocardial infarction, as recommended in the guidelines, has never been studied. To examine the effects of standard treatments of the myocardial infarction on the secretion of the most important ischemia/reperfusion cytokines. We used a murin macrophage model of inflammation (BMDM) to quantify the secretion of the main cytokines of ischemia/reperfusion (TNF-α, IL-6, IL-1α, IL-1β and IL-10). These macrophages were incubated alone, along with a treatment of each main class given after a myocardial infarction or with an association of pre-hospital phase treatments (aspirine, ticagrelor and unfractionned heparin). Secretion of the different cytokines was quantified using an ELISA testing. The standard treatments impact mostly IL-1β, which is known to be the most deleterious cytokine during ischemia/reperfusion. Its secretion is lowered by aspirin, the anti-Gp2b3a abciximab, and unfractionned heparin. The other treatments tested, including the low-weight molecular heparin enoxaparin, have no effect on IL-1β secretion. The standard treatments have only few effects on the secretion of the other cytokins. Aspirin, abciximab and unfractionned heparin have an important anti-IL-1β effect, reducing its secretion. This could explain the lack of efficacy of the specific anti-IL-1β treatments during the acute phase of myocardial infarction. These results should be confirmed using an in vivo murin model and a human in vitro model.
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