Metabolomics – a wide-open door to personalized treatment in chronic heart failure?

• Published in: International journal of cardiology Vol. 219; pp. 156 - 163
• Main Authors: Marcinkiewicz-Siemion, M, Ciborowski, M, Kretowski, A, Musial, W.J, Kaminski, K.A
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ireland Ltd 15-09-2016
• Subjects: Cardiac metabolism; Cardiovascular; Chronic Disease; Heart failure; Heart Failure - genetics; Heart Failure - metabolism; Heart Failure - therapy; High throughput techniques; Humans; Metabolic pathways; Metabolites; Metabolomics; Metabolomics - methods; Metabolomics - trends; Precision Medicine - methods; Precision Medicine - trends; Proteomics - methods; Proteomics - trends; Treatment Outcome; ACLI; B-type natriuretic protein; H-FABP c; single reaction monitoring; carnitine palmitoyltransferase-1; BNP; RAAS; LVEF; high throughput techniques; ADP; fatty acid translocase; capillary electrophoresis; G-6-P; renin-angiotensin-aldosterone system; FABP pm; phosphocreatine; metabolomics; adenosine diphosphate; cardiac hepathopathy; FAs; metabolic pathways; FATPs-6; heart failure; fatty acid transporter proteins 1; GLUTs; FATPs-1; multiple reaction monitoring; cardiac resynchronization therapy; plasma membrane-associated fatty acid-binding protein; MS; IR; N-terminal proBNP; transmembrane glucose transporters; LC-QQQ; liquid chromatography triple quadrupole; DCM; heart-type cytoplasmic fatty acid-binding protein; acute cardiogenic liver injury; SIM; ROS; dehydroepiandrosterone sulfate; CPT-1; fatty acid transporter proteins 6; fatty acids oxidation; CRT; left ventricle ejection fraction; peroxisome proliferator-activated receptors; cardiac metabolism; DHEA-S; MRM; gas chromatography; FAT/CD36; nicotinamide adenine dinucleotide; NADH; NT-proBNP; reactive oxygen species; glucose-6-phosphate; mass spectrometry; creatine kinase; GC; insulin resistance; PCr; dilated cardiomyopathy; CE; GLP-1; fatty acids; CH; CK; liquid chromatography; nuclear magnetic resonance; metabolites; PPARs; NMR; FAO; adenosine triphosphate; LC; glucagone-like peptide-1; ATP; HF; Metabolomics; Metabolites; High throughput techniques; FABPpm; Heart failure; Cardiac metabolism; H-FABPc; Metabolic pathways
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/j.ijcard.2016.06.022

Abstract Heart failure (HF) is a complex syndrome representing a final stage of various cardiovascular diseases. Despite significant improvement in the diagnosis and treatment (e.g. ACE-inhibitors, β-blockers, aldosterone antagonists, cardiac resynchronization therapy) of the disease, prognosis of optimally treated patients remains very serious and HF mortality is still unacceptably high. Therefore there is a strong need for further exploration of novel analytical methods, predictive and prognostic biomarkers and more personalized treatment. The metabolism of the failing heart being significantly impaired from its baseline state may be a future target not only for biomarker discovery but also for the pharmacologic intervention. However, an assessment of a particular, isolated metabolite or protein cannot be fully informative and makes a correct interpretation difficult. On the other hand, metabolites profile analysis may greatly assist investigator in an interpretation of the altered pathway dynamics, especially when combined with other lines of evidence (e.g. metabolites from the same pathway, transcriptomics, proteomics). Despite many prior studies on metabolism, the knowledge of peripheral and cardiac pathophysiological mechanisms responsible for the metabolic imbalance and progression of the disease is still insufficient. Metabolomics enabling comprehensive characterization of low molecular weight metabolites (e.g. lipids, sugars, organic acids, amino acids) that reflects the complete metabolic phenotype seems to be the key for further potential improvement in HF treatment (diet-based or biochemical-based). Will this -omics technique one day open a door to easy patients identification before they have a heart failure onset or its decompensation?