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Taken from WWW.pubmed.gov (testosterone studies)
Heart 2004;90:446-447
© 2004 by BMJ Publishing Group & British Cardiac Society
Testosterone treatment for men with chronic heart failure
P J Pugh1, R D Jones2, J N West1, T H Jones2 and K S Channer1
1 Department of Cardiology, Royal Hallamshire Hospital, Sheffield, UK
2 Academic Unit of Endocrinology, Division of Genomic Medicine, University of Sheffield Medical School, Sheffield, UK
Correspondence to:
Dr K S Channer
M131, Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK; Kevin.Channer@sth.nhs.uk
Chronic heart failure (CHF) is a disabling disease characterised by exercise intolerance and dyspnoea.
Disease progression arises from prolonged neurohormonal and pro-inflammatory cytokine activation and is
associated with a metabolic shift favouring catabolism, vasodilator incapacity, and loss of skeletal muscle
bulk and function. In men, androgens are important determinants of anabolic function and physical strength.
Androgens also possess anti-inflammatory and vasodilatory properties. In addition, testosterone has been
shown to augment cardiac output acutely in men with CHF. Low plasma concentrations of testosterone have
been described in men with CHF, and correlate positively with cardiac output. It was hypothesised that
relative hypotestosteronaemia could contribute to clinical features of muscle wasting and exercise
intolerance, inflammatory cytokine activation and impaired vasodilatation, and progression of heart
failure. This pilot study sought to determine whether testosterone treatment could improve exercise
capacity and symptoms in male patients with CHF.
DISCUSSION
We found significant improvements in exercise capacity and symptoms in men with heart failure following
treatment with testosterone. The mechanism of benefit is unclear. The small sample size limited our ability
to detect any significant impact of treatment on myocardial contractility, physical strength or humoral
factors. Alterations of skeletal muscle in heart failure patients include changes in muscle microstructure
and cellular energy handling and it may be that microscopic, but not macroscopic, muscle changes contributed
to improved exercise capacity and that these changes were undetectable by the imaging modality used. Also,
the population studied was relatively unselected and it may be that subpopulations of patients with cytokine
activation, cachexia, and sarcopenia may derive even greater benefit than that observed in this trial.
Further studies are warranted in patients with more advanced disease.
A trend to positive effect of testosterone on mood scores was observed. CHF patients have higher depression
scores than controls, as do testosterone deficient men, in whom replacement may reduce depressive symptoms. The improvement
in mood may have been related to improved functional capacity, vice versa or an independent phenomenon.
In conclusion, in men with CHF, 12 weeks of treatment with testosterone was safe, well tolerated, and led
to significant improvements in physical capacity and symptoms. The mechanism of action of testosterone and
confirmation of its safety and beneficial effect in selected patients require further evaluation in larger
clinical trials.
PMID: 16749913 [PubMed - as supplied by publisher]
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