Marcinkiewicz-Siemion M, Ciborowski M, Kretowski A, Musial W J, Kaminski K A
Cardiology Department, University Hospital, Bialystok, Poland.
Clinical Research Centre, Medical University of Bialystok, Poland.
Int J Cardiol. 2016 Sep 15;219:156-63. doi: 10.1016/j.ijcard.2016.06.022. Epub 2016 Jun 14.
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?
心力衰竭（HF）是一种复杂的综合征，代表各种心血管疾病的终末阶段。尽管在该疾病的诊断和治疗（如血管紧张素转换酶抑制剂、β受体阻滞剂、醛固酮拮抗剂、心脏再同步治疗）方面有了显著改善，但经过最佳治疗的患者的预后仍然非常严峻，HF的死亡率仍然高得令人无法接受。因此，迫切需要进一步探索新的分析方法、预测和预后生物标志物以及更个性化的治疗。衰竭心脏的代谢与其基线状态相比显著受损，这可能不仅是生物标志物发现的未来目标，也是药物干预的目标。然而，对一种特定的、孤立的代谢物或蛋白质的评估可能并不完全具有信息量，并且难以做出正确的解释。另一方面，代谢物谱分析可能极大地帮助研究人员解释改变的途径动态，特别是当与其他证据（如同一路径的代谢物、转录组学、蛋白质组学）相结合时。尽管之前有许多关于代谢的研究，但对于导致代谢失衡和疾病进展的外周和心脏病理生理机制的了解仍然不足。代谢组学能够全面表征反映完整代谢表型的低分子量代谢物（如脂质、糖类、有机酸、氨基酸），这似乎是HF治疗（基于饮食或基于生化）进一步潜在改善的关键。这种组学技术有朝一日会为在患者出现心力衰竭发作或失代偿之前轻松识别患者打开一扇门吗？
