The exact roles of circulating and intracardiac cytokines in acute decompensated heart failure remain unclear, necessitating larger investigational studies.
While proinflammatory cytokines play a known pathogenetic role in chronic heart failure, their specific role in acute decompensation requires further study.
In patients with chronic heart failure, ongoing myocardial injury partially results from activation of the inflammatory system, with production and release of proinflammatory cytokines, activation of the complement system, production of autoantibodies, overexpression of major histocompatibility complex molecules, and expression of adhesion molecules that may perpetuate the inflammatory state. Acute decompensated heart failure modifies the course of chronic heart failure and worsens outcomes via a combination of potential mechanisms, including neurohormonal activation, apoptosis, and the inflammatory cascade. Proinflammatory cytokines, including tumor necrosis factor-alpha and interleukin-6, play a pathogenetic role in chronic heart failure, and anti-inflammatory immune therapy is currently under investigation. In acute decompensation of chronic heart failure, the change in the inflammatory cytokine activation cascade is less clear. Larger investigational studies are needed to assess the exact roles of circulating and intracardiac cytokines in this particular patient population.
Chen et al. (Tue,) conducted a review in Acute heart failure. The exact roles of circulating and intracardiac cytokines in acute decompensated heart failure remain unclear, necessitating larger investigational studies.