Reappraising the role of chronic inflammatory burden in heart failure

Abstract

AbstractBackgroundHeart failure (HF) is a clinical syndrome associated with poor quality of life, substantial utilization of health care resources, and premature mortality. It is now considered to be the most urgent unmet medical need in the field of cardiovascular disease. Accumulated evidence suggested that comorbidity‐driven inflammation has emerged as a critical component of HF pathogenesis. Although anti‐inflammatory therapies have increased in popularity, very few effective treatments are still available. A comprehensive understanding of the interplay between chronic inflammation and its impact on HF will facilitate the identification of future therapeutic targets.MethodsA two‐sample Mendelian randomization study was conducted to assess the association between genetic liability for chronic inflammation and HF. By analyzing functional annotations and enrichment data, we were able to identify common pathophysiological mechanisms.ResultsThe present study did not provide evidence for chronic inflammation as the cause of HF and the reliability of the results was enhanced by the other three Mendelian randomization analysis methods. Functional annotations of genes and pathway enrichment analyses have indicated that chronic inflammation and HF share a common pathophysiology.ConclusionsThe associations between chronic inflammation and cardiovascular disease from observational studies may be explained by shared risk factors and comorbidities rather than direct effects.