Table 3.
A summary of the studies on lipidomics of lipoproteins reporting cardiovascular outcomes.
| Author, Country, Publication Year | Study Design | Number of Participants | Platform | Outcome | Findings | Adjusting for HDL-c, LDL-c, or TAGs |
|---|---|---|---|---|---|---|
| Yetukuri et al. [66], Finland, 2010 | Cross-sectional study in a survey | 47 participants (24 with low HDL-c and 23 with high HDL-c) | Lipidomics of HDLs measured by LC–MS, with 307 lipids identified. | Lipidome of HDL | Higher HDL-c was associated with lower TAGs (48:0, 48:1, 54:3), higher LPC (22:6, 18:1, 18:0), and higher SM (d18:1/16:0, d18:1/22:0, d18:1/24:1) in HDL. No correction for multiple testing. | - |
| Kostara et al. [61], Greece, 2017 | Cross-sectional study in hospital setting | 60 healthy participants (20 with low HDL-c, 20 with normal HDL-c, and 20 with high HDL-c) | Lipidomics of HDLs measured by NMR | Lipidome of HDL | Higher HDL-c was associated with lower TAGs, higher PUFA chain, and higher SM in HDL. No correction for multiple testing. | - |
| Kostara et al. [59,60], Greece, 2009, 2014 | Case–control study in hospital setting | 99 CHD cases (30 cases with mild CHD, 29 with moderate CHD, and 40 with severe CHD) and 60 controls | Lipidomics of HDL and non-HDL particles measured by NMR | Progression of CHD | Participants with more severe CHD presented higher levels of SFA chains in HDL and non-HDL particles, lower levels of PC and SM in HDL particles, and lower levels of PUFA chains in lipids in non-HDL particles. No correction for multiple testing. | - |
| Morgantini et al. [62], Italy, 2014 | Case–control study in hospital setting | 80 participants without CVD and 38 CVD cases | HETEs and HODEs in HDLs measured by LC–MS | CVD | HETEs (15-HETE, 12-HETE, 5-HETE) and HODEs (13-HODE, 9-HODE) content in HDLy were significantly higher in CVD cases in comparison to participants without CVD. No correction for multiple testing. | LDL-c |
| Sutter et al. [63], Switzerland, 2015 | Case–control study in hospital setting | 22 healthy participants and 45 CHD cases | 49 PCs, LPCs, and SMs, and 3 S1P in HDLs | CHD | Levels of PC-derived plasmalogens in HDLs (PC33:3, PC35:2, PC35:5) were significantly lower in CHD cases compared to controls. | - |
| Meikle et al. [64], Australia, 2019 | Case–control study in hospital setting | 47 participants with acute CHD and 83 with stable CHD | Lipidomics of HDLs and LDL by LC–MS | Subtypes of CHD | Level of lysophospholipids and plasmalogens in HDLs were significantly lower among acute CHD participants in comparison to patients with stable CHD. | Statin use |
| Cardner et al. [65], Switzerland, 2020 | Case–control study in hospital setting | 51 healthy subjects and 98 cases with T2D or CHD | Lipidomics of HDsL by ESI–MS | CHD or T2D | T2D or CHD cases presented higher PEs (38:5, 38:6, 40:7) and lower PIs (36:2, 34:2), PCs (36:2, 34:2), and CE 18:2. T2D cases had significantly lower levels of PCs (O-34:2, O-34:3, O-36:2, O-36:3), LPCs (18:2, 18:1, 18:0), and SMs (42:3 and 36:3). | - |
NMR: Nuclear magnetic resonance; LC–MS: Liquid chromatography–mass spectrometry; ESI-MS: Electrospray ionization–tandem mass spectrometry SM: Sphingomyelin; HETE: Hydroeicosatetraenoic acid; HODE: Hydroxyoctadecadienoic acids; S1P: Sphingosine-1-phosphate; PE: Phosphatidylethanolamines; PI: Phosphatidylinositols.