Key result
Elevated pre-PCI plasma levels of phosphatidylcholine, alkylphosphatidylcholine, and sphingomyelin were significantly associated with the no-reflow phenomenon in STEMI patients (p < 0.05).
Why the study?
The no-reflow phenomenon after primary PCI is a serious complication in acute STEMI patients, prompting investigation into lipidomic predictors.
Are specific plasma lipidomic profiles associated with the development of coronary no-reflow in STEMI patients undergoing primary PCI?
Observational (n=126)
Are specific plasma lipidomic profiles associated with the development of coronary no-reflow in STEMI patients undergoing primary PCI?
p-value: p=<0.05
Specific plasma lipid classes, including sphingomyelins and phosphatidylcholines, are elevated prior to PCI in STEMI patients who develop no-reflow, suggesting a role for dyslipidemia in this complication.
Lipid alterations may flag no-reflow risk after STEMI PCI; hypothesis-generating and requires prospective validation before any clinical use.
The ‘no-reflow’ phenomenon (NRP) after primary percutaneous coronary intervention (PCI) is a serious complication among acute ST-segment elevation myocardial infarction (STEMI) patients. Herein, a comprehensive lipidomics approach was used to quantify over 300 distinct molecular species in circulating plasma from 126 patients with STEMI before and after primary PCI. Our analysis showed that three lipid classes: phosphatidylcholine (PC), alkylphosphatidylcholine (PC(O)), and sphingomyelin (SM), were significantly elevated (p < 0.05) in no-reflow patients before primary PCI. The levels of individual fatty acids and total fatty acid levels were significantly lower (p < 0.05) in no-reflow subjects after PCI. The grouping of patients based on ECG ST-segment resolution (STR) also demonstrated the same trend, confirming the possible role of these differential lipids in the setting of no-reflow. Sphingomyelin species, SM 41:1 and SM 41:2, was invariably positively correlated with corrected TIMI frame count (CTFC) at pre-PCI and post-PCI. The plasma levels of SM 42:1 exhibited an inverse association (p < 0.05) consistently with tumor necrosis factor-alpha (TNF-α) at pre-PCI and post-PCI. In conclusion, we identified plasma lipid profiles that distinguish individuals at risk of no-reflow and provided novel insights into how dyslipidemia may contribute to NRP after primary PCI.
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Surendran et al. (2023) conducted an observational in acute ST-segment elevation myocardial infarction (STEMI) (n=126). Elevated pre-PCI plasma levels of phosphatidylcholine, alkylphosphatidylcholine, and sphingomyelin vs. Normal reflow was evaluated on No-reflow phenomenon (NRP) (p=<0.05). Elevated pre-PCI plasma levels of phosphatidylcholine, alkylphosphatidylcholine, and sphingomyelin were significantly associated with the no-reflow phenomenon in STEMI patients (p < 0.05).
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