Neuroendocrine effects on the heart and targets for therapeutic manipulation in heart failure.
Chronic heart failure (CHF) involves derangements in multiple neurohormonal axes leading to a procatabolic state and wasting syndrome associated with significant mortality. Catabolic abnormalities include excess catecholamines and glucocorticoids. Anabolic defects include deficiencies of sex steroids, insulin resistance, and growth hormone (GH) resistance. These abnormalities are also correlated with increased morbidity and mortality in CHF. Anabolic axes have been augmented in pilot studies in CHF with testosterone, GH, insulin-like growth factor-1, and GH secretagogues. Results have been varied although some treatments have been associated with improved surrogate endpoints. This review article explores the current understanding of metabolic derangements in CHF and highlights potential neuroendocrine treatment strategies.
Chaggar
Parminder S
PS
Northwest Heart and Transplant Centre, Wythenshawe Hospital, Manchester M23 9LT, UK. pchaggar@doctors.org.uk
Malkin
Chris J
CJ
Shaw
Steven M
SM
Williams
Simon G
SG
Channer
Kevin S
KS
D045930:Anabolic Agents / Q000378:metabolism; D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D005938:Glucocorticoids / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism; D019382:Human Growth Hormone / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance; D009490:Neurosecretory Systems / Q000187:drug effects* / Q000378:metabolism; D013256:Steroids / Q000378:metabolism
D045930:Anabolic Agents; D002395:Catecholamines; D005938:Glucocorticoids; D013256:Steroids; D019382:Human Growth Hormone