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Fingerprinting Cardiolipin in Leukocytes by Mass Spectrometry for a Rapid Diagnosis of Barth Syndrome
Published on: March 23, 2022
Circulating free fatty acid signatures discriminate myocardial infarction and systemic arterial hypertension
Simone Baldi1, Luis Alejandro Constantino-Jonapa2, Samuel Jaimez Alvarado2
1Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.
Background:
Gut microbiome (GM) dysbiosis and altered circulating free fatty acid (FFA) profiles have been implicated in cardiovascular diseases (CVDs), including systemic arterial hypertension (SAH) and ST-segment elevation myocardial infarction (STEMI). This study evaluated serum short-, medium-, and long-chain fatty acids (SCFAs, MCFAs, and LCFAs) in patients with SAH and STEMI compared with healthy controls (HCs), aiming to identify candidate biomarkers and potential mechanistic links between FFAs, the GM, and cardiovascular health.
Methods:
Serum samples from 47 STEMI patients, 17 SAH patients, and 28 HCs were analysed using gas chromatography-mass spectrometry.
Results:
Principal coordinates analyses (PCoA) showed significant group separation based on FFA profiles. Both STEMI and SAH patients exhibited increased total SCFA levels, with higher acetic, propionic, 2-methylbutyric, and isovaleric acids compared with HCs. Conversely, STEMI patients showed reduced isobutyric and valeric acids versus both HCs and SAH, and lower 2-methylbutyric acid relative to SAH. STEMI patients also had lower total MCFA levels, mainly due to reduced octanoic acid, while both patient groups showed increased hexanoic acid versus HCs. Additionally, STEMI patients showed elevated hexadecanoic acid and reduced octadecanoic acid compared with the other groups.Sparse partial least squares discriminant analysis (sPLS-DA) confirmed distinct FFA signatures: STEMI was characterised by increased propionic, hexadecanoic, and tetradecanoic acids, whereas SAH showed reduced isovaleric, 2-methylbutyric, hexanoic, and isobutyric acids.
Conclusions:
These findings indicate disease-specific circulating FFA patterns that may reflect metabolic alterations and underlying pathophysiological mechanisms.
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