Why the study?
Pro-inflammatory cytokines play a role in post-MI fibrosis, but the role of IL-12p40 and temporal cytokine changes in adverse cardiac remodeling after STEMI remains unclear.
Elevated levels of pro-inflammatory cytokines IL-12 and MMP-2 in the initial phase of STEMI are associated with subsequent adverse cardiac remodeling.
IL-12p40 dynamics may mark post-STEMI remodeling risk; leaves open whether targeting it alters outcomes.
Introduction: Increasing evidence supports the view that pro-inflammatory cytokines play a role in fibrosis after myocardial infarction (MI). It has been suggested that interleukin (IL)-12p40, a pro-inflammatory cytokine, can induce interferon γ (IFN-γ) and matrix metalloproteinase (MMP). However, the role of IL-12p40 in adverse cardiac remodeling (AR) after ST-elevation MI (STEMI) is unclear. Aim: To examine the role of temporal changes of pro-inflammatory cytokines in the development of post-STEMI AR. Material and methods: A total of 43 patients with STEMI for the first time ever were prospectively analyzed. In cardiac magnetic resonance imaging at 6 months after STEMI, a decrease of left ventricular end-diastolic volume by ≥ 12% was defined as reverse cardiac remodeling (RR), and a 12% increase was defined as AR. Cytokine concentrations were measured on the first day (baseline) and 2 weeks after STEMI. Results: = 0.035). Conclusions: In the initial phase of MI, greater release of pro-inflammatory cytokines was associated with increased MMP-2 levels. Elevated expression of IL-12 and MMP-2 had an independent association with AR. This may be related to the excessive inflammatory response in the initial phase of MI.
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Altıntaş et al. (2022) studied this question.
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