Heart failure (HF) is characterized by a progressive decline in cardiac function and represents one of the largest health burdens worldwide. Clinically, 2 major types of HF are distinguished based on the left ventricular ejection fraction (EF): HF with reduced EF and HF with preserved EF. While both types share several risk factors and features of adverse cardiac remodeling, unique hallmarks beyond ejection fraction that distinguish these etiologies also exist. These differences may explain the fact that approved therapies for HF with reduced EF are largely ineffective in patients suffering from HF with preserved EF. Improving our understanding of the distinct cellular and molecular mechanisms is crucial for the development of better treatment strategies. This article reviews the knowledge of the immunologic mechanisms underlying HF with reduced and preserved EF and discusses how the different immune profiles elicited may identify attractive therapeutic targets for these conditions. We review the literature on the reported mechanisms of adverse cardiac remodeling in HF with reduced and preserved EF, as well as the immune mechanisms involved. We discuss how the knowledge gained from preclinical models of the complex syndrome of HF as well as from clinical data obtained from patients may translate to a better understanding of HF and result in specific treatments for these conditions in humans.

中文翻译：

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射血分数减少和保留的心力衰竭中的心肌炎症。


心力衰竭（HF）的特点是心脏功能进行性下降，是全球最大的健康负担之一。临床上，根据左心室射血分数 (EF)，可区分 2 种主要类型的心力衰竭：EF 降低的心力衰竭和 EF 保留的心力衰竭。虽然这两种类型都有一些不良心脏重塑的危险因素和特征，但除了射血分数之外还存在区分这些病因的独特特征。这些差异可能解释了这样一个事实：已批准的 EF 降低的心力衰竭治疗方法对于 EF 保留的心力衰竭患者基本上无效。提高我们对不同细胞和分子机制的理解对于制定更好的治疗策略至关重要。本文回顾了 EF 减少和保留的 HF 背后的免疫机制的知识，并讨论了所引发的不同免疫特征如何识别这些疾病的有吸引力的治疗靶点。我们回顾了有关 EF 减少和保留的心力衰竭中不良心脏重塑机制的文献，以及所涉及的免疫机制。我们讨论从心力衰竭复杂综合征的临床前模型以及从患者获得的临床数据中获得的知识如何转化为对心力衰竭的更好理解，并导致针对人类这些疾病的具体治疗。