Despite promising experimental data, large-scale clinical trials targeting inflammatory mediators in chronic heart failure have largely failed to demonstrate significant clinical benefits.
This review highlights the translational perspective on inflammation in heart failure, noting the failure of early anti-cytokine trials and discussing promising novel therapeutic targets.
The prevalence of chronic heart failure is still increasing making it a major health issue in the 21st century. Tremendous evidence has emerged over the past decades that heart failure is associated with a wide array of mechanisms subsumed under the term "inflammation". Based on the great success of immuno-suppressive treatments in auto-immunity and transplantation, clinical trials were launched targeting inflammatory mediators in patients with chronic heart failure. However, they widely lacked positive outcomes. The failure of the initial study program directed against tumor necrosis factor-α led to the search for alternative therapeutic targets involving a broader spectrum of mechanisms besides cytokines. We here provide an overview of the current knowledge on immune activation in chronic heart failure of different etiologies, summarize clinical studies in the field, address unresolved key questions, and highlight some promising novel therapeutic targets for clinical trials from a translational basic science and clinical perspective.
Hofmann et al. (Wed,) conducted a review in Chronic heart failure. Immuno-modulatory treatments was evaluated. Despite promising experimental data, large-scale clinical trials targeting inflammatory mediators in chronic heart failure have largely failed to demonstrate significant clinical benefits.