Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction.
D, L., L, D., Z, W., Y, H., C, P., H, L., & Y, Z. (2026). Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction.. Vascular health and risk management. https://doi.org/10.2147/VHRM.S606866
D L, L D, Z W, Y H, C P, H L, et al. Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction.. Vascular health and risk management. 2026; doi: 10.2147/VHRM.S606866
D L, L D, Z W, et al. Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction.[J]. Vascular health and risk management. 2026. DOI: 10.2147/VHRM.S606866.
@article{d2026,
author = {Lu D and Deng L and Wang Z and Hu Y and Pan C and Lu H and Zhou Y},
title = {Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction.},
journal = {Vascular health and risk management},
year = {2026},
doi = {10.2147/VHRM.S606866},
note = {PMID: 42483693},
}
TY - JOUR AU - Lu D AU - Deng L AU - Wang Z AU - Hu Y AU - Pan C AU - Lu H AU - Zhou Y TI - Lipidomic Profiling and Biological Aging in Patients with Coronary Microvascular Dysfunction. T2 - Vascular health and risk management PY - 2026 DO - 10.2147/VHRM.S606866 AN - PMID:42483693 ER -
BACKGROUND: Coronary microvascular dysfunction (CMD) was frequently encountered in patients with angina in the absence of epicardial coronary stenosis. CMD was associated with adverse outcomes while the etiology was unclear. OBJECTIVE: In this study, we aimed to investigate the association between lipidomic abnormalities, biological aging and CMD. METHODS: We consecutively enrolled 43 patients with angina exhibiting no epicardial coronary stenosis on angiography. CMD was defined by a coronary angiography-derived index of microvascular resistance (caIMR) >25. Targeted lipidomic profiling quantified 781 lipids. PhenoAge was calculated from clinical parameters. Using machine learning, lipidomic data and clinical characteristics were screened to identify candidate biomarkers. RESULTS: There were 25 patients having CMD with the mean caIMR of 34.0 (Interquartile range [IQR], 31.0-36.5), in contrast to 23.0 (IQR, 19.0-24.5) in the control group. Patients with CMD had substantially older PhenoAge (61 vs 52, p = 0.002). Forty-eight lipid species were dysregulated in patients with CMD, which predominantly belonged to triacylglycerol (TAG). PhenoAge, triglyceride glucose index, hypertension, TAG47:2-FA14:0, TAG48:4-FA18:1 and phosphatidylcholine (18:1/20:3) were independent risk factors of CMD. Incorporating dysregulated lipids significantly improved CMD prediction compared to traditional clinical factors alone (area under the curve, 0.94 vs 0.86, p < 0.05). CONCLUSION: PhenoAge acceleration and dysregulated lipidome were associated with CMD. Larger-scale studies and external validation are needed in the future.