Key result
Myocardial infarction is linked to myocardial phospholipid depletion and neutral lipid accumulation.
Observational
Human myocardial infarction is associated with profound myocardial lipid remodeling characterized by a loss of structural polyunsaturated phospholipids and an accumulation of saturated triacylglycerols.
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Post-MI atrial omega-3 PUFA lipid depletion is hypothesis-generating; leaves open any therapeutic or prognostic role pending prospective studies.
Myocardial lipid remodeling in myocardial infarction (MI) remains insufficiently characterized in human myocardium. Using liquid chromatography–mass spectrometry, we analyzed left atrial appendage tissue from patients with and without MI undergoing cardiac surgery. MI was characterized by reduced phospholipid species containing omega-3 polyunsaturated fatty acids (PUFAs) and myristic acid, together with reduced diacylglycerol species containing omega-3 PUFAs. Reduced phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, and plasmalogens were observed, whereas triacylglycerols were enriched. Loss of polyunsaturated phospholipids and accumulation of relatively saturated triacylglycerols indicate a shift toward neutral lipid storage in human MI myocardium.
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Shiozawa et al. (2026) conducted an observational in Myocardial infarction. Myocardial infarction vs. No myocardial infarction was evaluated on Myocardial lipid remodeling (lipid species composition). Myocardial infarction was associated with a loss of polyunsaturated phospholipids and an accumulation of triacylglycerols, indicating a shift toward neutral lipid storage in human myocardium.
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