The observation that heart failure with reduced ejection fraction is associated with elevated circulating levels of pro-inflammatory cytokines opened a new area of research that has revealed a potentially important role for the immune system in the pathogenesis of heart failure. However, until the publication in 2019 of the CANTOS trial findings on heart failure outcomes, all attempts to target inflammation in the heart failure setting in phase III clinical trials resulted in neutral effects or worsening of clinical outcomes. This lack of positive results in turn prompted questions on whether inflammation is a cause or consequence of heart failure. This Review summarizes the latest developments in our understanding of the role of the innate and adaptive immune systems in the pathogenesis of heart failure, and highlights the results of phase III clinical trials of therapies targeting inflammatory processes in the heart failure setting, such as anti-inflammatory and immunomodulatory strategies. The most recent of these studies, the CANTOS trial, raises the exciting possibility that, in the foreseeable future, we might be able to identify those patients with heart failure who have a cardio-inflammatory phenotype and will thus benefit from therapies targeting inflammation.

中文翻译：

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重新评估炎症在心力衰竭中的作用。

射血分数降低的心力衰竭与促炎细胞因子循环水平升高相关的观察开辟了一个新的研究领域，揭示了免疫系统在心力衰竭发病机制中的潜在重要作用。然而，在 2019 年 CANTOS 心力衰竭结局试验结果发表之前，所有针对 III 期临床试验中心力衰竭环境炎症的尝试都导致了中性效应或临床结局恶化。这种缺乏积极结果反过来又引发了关于炎症是心力衰竭的原因还是后果的问题。本综述总结了我们对先天性和适应性免疫系统在心力衰竭发病机制中作用的理解的最新进展，并强调针对心力衰竭环境中炎症过程的疗法的 III 期临床试验结果，例如抗炎和免疫调节策略。这些研究中最近的一项，即 CANTOS 试验，提出了一种令人兴奋的可能性，即在可预见的未来，我们可能能够识别出那些具有心脏炎症表型的心力衰竭患者，从而从针对炎症的治疗中获益。