Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Norway; Faculty of Medicine, University of Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Norway; KG Jebsen Thrombosis Research and Expertise Center, N-9037 Tromsø, Norway.
Department of Cardiology, Oslo University Hospital Rikshospitalet, Norway; Faculty of Medicine, University of Oslo, Norway; KG Jebsen Cardiac Research Center and Center for Heart Failure Research, University of Oslo, Norway.
Clin Chim Acta. 2015 Mar 30;443:71-7. doi: 10.1016/j.cca.2014.09.001. Epub 2014 Sep 6.
Inflammation has been implicated in the pathogenesis of heart failure (HF). In addition to their direct involvement as mediators in the pathogenesis of HF, inflammatory cytokines and related mediators could also be suitable markers for risk stratification and prognostication in HF patients. Many reports have suggested that inflammatory cytokines may predict adverse outcome in these patients. However, most studies have been limited in sample size and lacking full adjustment with the most recent and strongest biochemical predictor such as NT-proBNP and high sensitivity troponins. Furthermore, a number of pre-analytical and analytical aspects of cytokine measurements may limit their use as biomarkers. This review focuses on technical, informative and practical considerations concerning the clinical use of inflammatory cytokines as prognostic biomarkers in HF. We focus on the predictive value of tumor necrosis factor (TNF) α, the TNF family receptors sTNFR1 and osteoprotegerin, interleukin (IL)-6 and its receptor gp130, the chemokines MCP-1, IL-8, CXCL16 and CCL21 and the pentraxin PTX-3 in larger prospective fully adjusted studies. No single inflammatory cytokine provides sufficient discrimination to justify the transition to everyday clinical use as a prognosticator in HF. However, while subjecting potential new HF markers to rigorous comparisons with "gold-standard" markers, such as NT-proBNP, using receiver operating characteristics (ROCs) and HF risk models, makes sense from a clinical standpoint, it may pose a threat to a broadening of mechanistic insight if the new markers are dismissed solely on account of lower statistical power.
炎症与心力衰竭（HF）的发病机制有关。除了作为 HF 发病机制的直接介质外，炎症细胞因子和相关介质也可能是 HF 患者风险分层和预后的合适标志物。许多报告表明，炎症细胞因子可能预测这些患者的不良预后。然而，大多数研究在样本量方面受到限制，并且缺乏最新和最强的生化预测因子（如 NT-proBNP 和高敏肌钙蛋白）的充分调整。此外，细胞因子测量的一些分析前和分析方面可能限制其作为生物标志物的使用。
本综述重点介绍了炎症细胞因子作为 HF 预后生物标志物的临床应用的技术、信息和实用方面的考虑因素。我们重点关注肿瘤坏死因子（TNF）α、TNF 家族受体 sTNFR1 和骨保护素、白细胞介素（IL）-6 及其受体 gp130、趋化因子 MCP-1、IL-8、CXCL16 和 CCL21 以及 pentraxin PTX-3 在更大的前瞻性完全调整研究中的预测价值。
没有单一的炎症细胞因子提供足够的区分度，不足以证明其作为 HF 预后标志物过渡到日常临床使用是合理的。然而，从临床角度来看，将潜在的新 HF 标志物与 NT-proBNP 等“金标准”标志物进行严格比较，并使用接收者操作特征（ROC）和 HF 风险模型进行比较是有意义的，但如果仅由于统计效力较低而排除新标志物，可能会对拓宽机制见解构成威胁。
