Why the study?
Past studies raised the question of whether inflammation is a constant condition or triggered in different amounts according to heart failure phenotype, prompting a review to identify proinflammatory cytokines as independent risk factors.
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This review assesses current evidence on the inflammatory activation cascade in heart failure and explores future targets for inflammatory response modulation to impact disease progression.
Chronic heart failure is a terminal point of a vast majority of cardiac or extracardiac causes affecting around 1-2% of the global population and more than 10% of the people above the age of 65. Inflammation is persistently associated with chronic diseases, contributing in many cases to the progression of disease. Even in a low inflammatory state, past studies raised the question of whether inflammation is a constant condition, or if it is, rather, triggered in different amounts, according to the phenotype of heart failure. By evaluating the results of clinical studies which focused on proinflammatory cytokines, this review aims to identify the ones that are independent risk factors for heart failure decompensation or cardiovascular death. This review assessed the current evidence concerning the inflammatory activation cascade, but also future possible targets for inflammatory response modulation, which can further impact the course of heart failure.
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Arvunescu et al. (2023) studied this question.
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