Why the study?
Despite the recognized role of inflammation in heart failure pathophysiology, clinical trials of anti-inflammatory agents have shown inconclusive or contradictory results.
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This review emphasizes the complex interplay between inflammation and neurohormonal activation in heart failure, underscoring the need to identify specific inflammatory pathways as therapeutic targets given the inconclusive results of past trials.
The pivotal role of inflammation in the pathophysiology of heart-failure (HF) development and progression has long been recognized. High blood levels of pro-inflammatory and inflammatory markers are present and associated with adverse outcomes in patients with HF. In addition, there seems to be an interrelation between inflammation and neurohormonal activation, the cornerstone of HF pathophysiology and management. However, clinical trials involving anti-inflammatory agents have shown inconclusive or even contradictory results in improving HF outcomes. In the present review, we try to shed some light on the reciprocal relationship between inflammation and HF in an attempt to identify the central regulating factors, such as inflammatory cells and soluble mediators and the related inflammatory pathways as potential therapeutic targets.
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Paraskevaidis et al. (2023) studied this question.
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