Mann Douglas L
From the Division of Cardiology, Department of Medicine, Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, MO.
Circ Res. 2015 Mar 27;116(7):1254-68. doi: 10.1161/CIRCRESAHA.116.302317.
Elevated levels of inflammatory mediators have been identified in patients with heart failure, including heart failure with reduced and preserved ejection fraction, as well as acute decompensated heart failure. Moreover, experimental studies have shown repeatedly that activation of inflammation in the heart provokes left ventricular remodeling and left ventricular dysfunction. Nonetheless, phase III clinical trials that have attempted to antagonize inflammatory mediators have been negative with respect to the primary end points of the trials, and in some patients, resulted in worsening heart failure or death. The following review will discuss how recent developments in the field of innate immunity have advanced our understanding of the role of inflammation in the pathogenesis of heart failure and will discuss the negative outcomes of the existing clinical trials in light of this new information.
在心力衰竭患者中已发现炎症介质水平升高,包括射血分数降低和保留的心力衰竭患者,以及急性失代偿性心力衰竭患者。此外,实验研究反复表明,心脏炎症的激活会引发左心室重构和左心室功能障碍。尽管如此,试图拮抗炎症介质的III期临床试验在试验的主要终点方面均为阴性,并且在一些患者中,导致心力衰竭恶化或死亡。以下综述将讨论固有免疫领域的最新进展如何增进我们对炎症在心力衰竭发病机制中作用的理解,并将根据这些新信息讨论现有临床试验的阴性结果。