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Review Article| Volume 201, e1-e12, December 15, 2015

Cardiac cachexia: hic et nunc

hic et nunc” — here and now
Published:October 15, 2015DOI:https://doi.org/10.1016/j.ijcard.2015.10.115

      Highlights

      • epidemiological data about prevalence of cardiac cachexia remain scarce
      • patophysiology of cardiac cachexia is complex and multifactorial
      • diagnostic and prognostic biomarkers are under investigation in cardiac cachexia
      • no evidence based strategy for cachexia available but many interventions in clinical trials

      Abstract

      Cardiac cachexia (CC) is the clinical entity at the end of chronic natural course of heart failure (HF). Despite the efforts, even the most recent definition of cardiac cachexia has been challenged, more precisely the addition of new criteria on top of obligatory weight loss. The pathophysiology of CC is complex and multifactorial. Better understanding of pathophysiological pathways in body wasting will contribute to establish potentially novel treatment strategies. The complex biochemical network related with CC and HF pathophysiology underlines that a single biomarker cannot reflect all of the features of the disease. Biomarkers that could pick-up the changes in body composition before they convey into clinical manifestations of CC would be of great importance. The development of preventive and therapeutic strategies against cachexia, sarcopenia and wasting disorders is perceived as an urgent need by healthcare professionals. The treatment of body wasting remains an unresolved challenge to this day. As CC is a multifactorial disorder, it is unlikely that any single agent will be completely effective in treating this condition. Among all investigated therapeutic strategies, aerobic exercise training in HF patients is the most proved to counteract skeletal muscle wasting and is recommended by treatment guidelines for HF.

      Abbreviations:

      ActRIIB (Activin type II B receptors), AET (Aerobic exercise training), BCAA (Branched chain amino acid), C6M (MMP-generated degradation fragment of collagen 6), CAF (C-terminal agrin fragment), CC (cardiac cachexia), GDF15 (growth differentiation factor 15), HF (heart failure), IC6 (type VI collagen N-terminal globular domain epitope), IGF-1 (Insulin-like growth factor 1), P3NP (N-terminal propeptide of type III procollagen), RAAS (renin–angiotensin–aldosterone axis), SNS (sympathetic nervous system), sTNFRs (Soluble tumor necrosis factor receptors (sTNFRs)), TNF-α (tumor necrosis factor alpha), UPP (ubiquitin–proteasome pathway)

      Keywords

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