Plasma lipid remodeling during the early recovery phase after myocardial infarction

Acute myocardial infarction (MI) induces extensive disturbances in lipid homeostasis; however, most lipidomic studies have focused on the acute hours-to-days phase or the chronic months-to-years period. To the best of our knowledge, this is the first study to characterize plasma lipidomic patterns specifically during the early recovery window (3–6 weeks post-MI), a clinically stable yet biochemically active stage of healing. We compared plasma lipid profiles—including phospholipids, sphingomyelins (SMs), and ceramides (Cers)—in acute MI patients, early-recovery patients, and healthy controls. LC-MS lipidomics revealed marked depletion of polyunsaturated phosphatidylcholines (PCs) and plasmalogens during MI. During recovery, PC-derived plasmalogens showed partial restoration, whereas PE-derived plasmalogens remained suppressed. Lysophospholipids were elevated acutely but normalized by 3–6 weeks, coinciding with improvements in systemic inflammatory markers. Saturated and monounsaturated PCs increased during recovery. Distinct alterations were also observed in sphingolipids. Ceramide species remained elevated during early recovery, while SM levels partially declined. Pathway analysis indicated that MI most strongly disrupted glycerophospholipid metabolism, arachidonic acid metabolism, and sphingolipid-related pathways, whereas the recovery group showed only partial metabolic normalization. By focusing on an underexplored transitional window, this study provides descriptive insight into post-infarction lipid remodeling and suggests that plasma lipidomics may capture both acute injury and early recovery-related metabolic states under contemporary clinical management.