Effects of Pericardial Fluid EVs on Coronary Endothelial Lipids via LC-MS

Operating under the opinion that there is alack of understanding of how factors in the pericardial fluid (PF) of patients with coronary artery disease (CAD) can influence the lipidome of coronary artery endothelium, researchers explored the impact of PF-derived extracellular vesicles (EVs) on the lipidome of human coronary artery endothelial cells (HCAECs) in patients with CAD. HCAECs were exposed to PF-derived small EVs collected from a trio of patients each with and without CAD, and untargeted liquid chromatography-mass spectrometry (LC-MS) was subsequently used to determine the lipidome of the HCAECs. A paper based on this research was published in CJC Open.¹

What Inspired This Research?

Heart disease caused by CAD affects millions of people around the world every year.² While endothelial cells forming the inner lining of the coronary arteries can be damaged by several factors, including atherosclerosis, the researchers previously published an article showing that the PF from patients with CAD can promote heart tissue scarring through the transforming growth factor beta pathway.³ Since the outer coronary arteries are always in contact with PF, the teams believe it to be likely that substances in this fluid can affect how HCAECs function and respond to treatments.¹

In addition, though particles in the fluid surrounding the heart may alter how blood vessels process fats in heart disease patients, because fat analysis is highly complex, the researchers believed that knowledge concerning that analysis currently lags. Believing that studying specific fat molecules, rather than just broad categories, is essential for truly understanding clogged arteries and developing better heart disease treatments inspired the team to conduct this research.¹

What Did the Researchers Discover?

The researchers identified a total of 1043 lipid species were identified in untreated HCAECs and HCAECs treated with PF-derived small EVs. The predominant lipid types were glycerophospholipids, glycerolipids, and sphingolipids. Quantification of individual lipid classes showed HCAECs treated with PF EVs showed reduced summed intensities of lysophosphatidylglycerols and diacylglycerophosphoinositols compared to untreated controls. Treatment with PF EVs derived from Non-CAD patients led to an increase in sphingoid bases, whereas this effect was not observed with CAD-derived PF EVs. Both Non-CAD and CAD PF EV treatments resulted in elevated prenol lipids compared to controls.¹

The authors of the paper reported¹they found that “EVs derived from the PF of patients with CAD can potentially influence the lipidome of HCAECs. We also show that PF-derived EVs potentially have the capacity to alter the lipid metabolism of HCAECs. Finally, although limited by a relatively small sample size, we demonstrate that a specific population of EVs can potentially induce changes in selective lipid species in HCAECs.” The research team recommends that future work build on these observations and determine whether they have any significant clinical and therapeutic implications.¹

Read More on Similar Topics

UHPLC and LC-MS/MS Profiling Reveals Gut Microbiota Dysbiosis and Novel Biomarkers in Coronary Heart Disease

Study: HPLC-MS/MS Assay Validated for Cardiovascular Metabolomics

References

1. Fatehi Hassanabad, A.; Meechem, M. B.; Chen, Y. L. et al. Pericardial Fluid-Derived Small Extracellular Vesicles from Patients with Coronary Disease Alter the Lipidome of Human Coronary Artery Endothelium. CJC Open 2025, 8 (4), 481-492. DOI: 10.1016/j.cjco.2025.12.010
2. 2.Shi, H.; Xia, Y.; Cheng, Y. et al. Global Burden of Ischaemic Heart Disease from 2022 to 2050: Projections of Incidence, Prevalence, Deaths, and Disability-Adjusted Life Years. Eur Heart J Qual Care Clin Outcomes 2025, 11 (4), 355-366. DOI: 10.1093/ehjqcco/qcae049
3. Fatehi Hassanabad, A.; Belke, D. D.; Gordon, P. M. K. et al. Pericardial Fluid of Patients With Coronary Artery Disease Can Drive Fibrosis Via TGF-Beta Pathway. JACC Basic Transl Sci. 2024, 9 (11),1329-1344. DOI: 10.1016/j.jacbts.2024.06.007