Key result
Early STEMI reperfusion links to a ~2-fold acute rise in 16 lipid biomarkers.
Why the study?
Reperfusion injury is a leading cause of myocardial cell death and heart failure, and new lipid biomarkers are needed to optimize diagnosis and assess severity of myocardial ischemia reperfusion injury.
Observational (n=40)
No
Effect estimate: 1.5- to 2-fold increase
Should not guide STEMI management now; leaves open validation of these lipids as reperfusion biomarkers.
BACKGROUND Reperfusion injury is one of the leading causes of myocardial cell death and heart failure. This study was performed to identify new candidate lipid biomarkers for the purpose of optimizing the diagnosis of myocardial ischemia reperfusion (I/R) injury, assessing the severity of myocardial I/R injury and trying to find the novel mechanism related to lipids. MATERIAL AND METHODS Forty patients who were diagnosed with ST-segment elevation myocardial infarction (STEMI) were randomly selected for this study. Serum samples from all the patients with STEMI were collected at 3 time periods: after STEMI diagnosis but prior to reperfusion (T0); and then at 2 hours (T2) and 24 hours (T24) after the end of the percutaneous coronary intervention procedure. Plasma lipidomics profiling analysis was performed to identify the lipid metabolic signatures of myocardial I/R injury using lipidomics. RESULTS Sixteen types of potential lipid biomarkers at different time periods (T0, T2, T24) were identified by using lipidomics technology. The T0 time periods exhibited 16 differentially metabolized lipid peaks in the patients after STEMI diagnosis but prior to reperfusion. With the increase of reperfusion times, the contents of these 16 lipid biomarkers decreased gradually, but there was a 1.5- to 2-fold increase of those 16 lipid biomarkers contents at T2 compared with T24. CONCLUSIONS Lipidomics analysis demonstrated differential change before and after reperfusion, suggesting a potential role of some of these lipids as biomarkers for optimizing the diagnosis of myocardial I/R, as well as for therapeutic targets against myocardial I/R injury.
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Feng et al. (2018) conducted an observational in ST-segment elevation myocardial infarction (STEMI) (n=40). Myocardial reperfusion via PCI vs. Before reperfusion (T0) was evaluated on Differentially metabolized lipid peaks before and after reperfusion (1.5- to 2-fold increase).
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