Targeted circulating lipid mediators and immune cell gene transcripts after ST-elevation myocardial infarction.

Residual inflammation drives atherogenesis to atherosclerosis and myocardial infarction, which triggers acute inflammation. In preclinical studies, polyunsaturated fatty acids-derived specialized pro-resolving mediators (SPMs) have been shown to promote recovery after myocardial infarction (MI), in contrast to proinflammatory lipid mediators (PIMs). However, the dynamic changes of lipid mediators after ST-elevation myocardial infarction (STEMI), particularly after percutaneous coronary intervention (PCI) and respective gene transcripts, are poorly understood. Therefore, the study aimed to assess the early dynamic changes in circulating lipid mediators and lipid pathway transcripts in patients with STEMI who undergo PCI. In this prospective observational clinical study, patients with STEMI ( = 10) and control subjects ( = 6) were included. Plasma samples for lipid mediator profiling (targeted oxylipids) and whole blood for inflammation-related transcript expression were collected at baseline before PCI, 2-, and 24-h post-PCI. A total of 10 patients with STEMI received PCI with a mean age of 53.3 yr, 90% male. Linoleic acid and docosapentaenoic acid levels were higher in patients with STEMI. A subset of PIM levels [hydroxyeicosatetraenoic acids, prostaglandin (PG)E] was elevated at the baseline, with a subsequent decrease in circulating levels at 2 h after PCI [thromboxanes, leukotriene B4 (LTB), 20-hydroxy-LTB]. A subset of SPM levels was elevated at the baseline of STEMI suggestive overlap of inflammation-resolution signaling. The temporal kinetics of lipid mediators showed that both the initiation of inflammation and the resolution process start simultaneously and continue as an endogenous repair mechanism during STEMI. Therefore, approaches to increase these endogenous bioactive resolution mediators content and/or efficacy before PCI should be considered in treating patients with MI. Polyunsaturated fatty acids-derived SPMs are decisive in myocardial infarction (MI) recovery, contrasting with proinflammatory lipid mediators (PIMs). A study on early lipid changes post-percutaneous coronary intervention (PCI) in patients with STEMI shows baseline elevation and post-PCI decrease in PIMs, whereas some SPM levels remain elevated. Findings highlight simultaneous inflammation and resolution in STEMI, emphasizing the need to enhance endogenous repair processes before PCI for better MI treatment.