Metabolic Disturbances Identified in Plasma Samples from ST-Segment Elevation Myocardial Infarction Patients

• Published in: Disease markers Vol. 2019; no. 2019; pp. 1 - 10
• Main Authors: Resende, Rodrigo R., Pinto, Mauro C. X., Batista, Josimar Marques, Sandrim, Valéria C., Santos, Anderson Kenedy, Goulart, Vânia A. M., Cameron, Luiz Cláudio
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2019; Hindawi; John Wiley & Sons, Inc
• Subjects: Adult; Aged; Aged, 80 and over; Amines; Analysis; Apoptosis; Biogenic amines; Biogenic Amines - blood; Bioindicators; Biomarkers; Biomarkers - blood; Blood coagulation; Brazil; Cardiac patients; Cardiology; Coronary artery; Coronary artery disease; Coronary vessels; Diagnosis; Electrocardiography; Enzymes; Ethylenediaminetetraacetic acid; Fatty acids; Female; Flow injection analysis; Gene expression; Health aspects; Heart; Heart attack; Heart attacks; Heart diseases; High performance liquid chromatography; Humans; Linolenic acid; Linolenic acids; Liquid chromatography; Male; Mass spectrometry; Mass spectroscopy; Medical imaging; Metabolism; Metabolites; Metabolome; Metabolomics; Middle Aged; Morbidity; Mortality; Multivariate analysis; Myocardial infarction; Occlusion; Omega-3 fatty acids; Phosphatidylcholines - blood; Proteins; Sphingomyelins - blood; ST Elevation Myocardial Infarction - blood; Transcription; Veins & arteries; Brazil
• ISSN: 0278-0240; 1875-8630; 1875-8630
• DOI: 10.1155/2019/7676189

ST-segment elevation myocardial infarction (STEMI) is the most severe form of myocardial infarction (MI) and the main contributor to morbidity and mortality caused by MI worldwide. Frequently, STEMI is caused by complete and persistent occlusion of a coronary artery by a blood clot, which promotes heart damage. STEMI impairment triggers changes in gene transcription, protein expression, and metabolite concentrations, which grants a biosignature to the heart dysfunction. There is a major interest in identifying novel biomarkers that could improve the diagnosis of STEMI. In this study, the phenotypic characterization of STEMI patients (n=15) and healthy individuals (n=19) was performed, using a target metabolomics approach. Plasma samples were analyzed by UPLC-MS/MS (ultra-high-performance liquid chromatography-tandem mass spectrometry) and FIA-MS (MS-based flow injection analysis). The goal was to identify novel plasma biomarkers and metabolic signatures underlying STEMI. Concentrations of phosphatidylcholines, lysophosphatidylcholines, sphingomyelins, and biogenic amines were altered in STEMI patients in relation to healthy subjects. Also, after multivariate analysis, it was possible to identify alterations in the glycerophospholipids, alpha-linolenic acid, and sphingolipid metabolisms in STEMI patients.