QJM, Vol 91, Issue 3 199-203, Copyright © 1998 by Oxford University Press
SD Anker, M Volterrani, KR Egerer, CV Felton, WJ Kox, PA Poole-Wilson and AJ Coats
Tumour necrosis factor alpha (TNF alpha) is increased in patients with
cardiac cachexia, a condition associated with reduced peripheral blood flow
both at rest and after interventions causing vasodilation. By contrast, in
patients with chronic heart failure (CHF), higher TNF levels are associated
with a greater capacity for vasodilation in the arm. To clarify the
relationship between peripheral blood flow and TNF in CHF, we studied the
relation between TNF alpha and blood flow in the leg (plethysmography, post
maximal exercise and 5 min ischaemia) in 34 patients (age 63 +/- 2 years,
ejection fraction 29 +/- 3%, peak VO2 16.6 +/- 1.1 ml/kg/min, mean +/-
SEM). Peak leg blood flow correlated significantly with total TNF alpha (r
= 0.68, p < 0.0001, peak VO2 (r = 0.54), and soluble TNF receptors 1 (r
= 0.56) and 2 (r = 0.52, all p < 0.002). TNF alpha, soluble TNF
receptors 1 and 2 and aldosterone correlated with peak blood flow
independently of age, ejection fraction, peak VO2 and functional NYHA
class. TNF alpha was the only parameter that showed strong correlations for
peak blood flow in all clinically relevant subgroups (severe vs. mild,
ischaemic vs. dilated, cachectic vs. non-cachectic patients). This study
shows a close and inverse relationship between peak leg blood flow and the
plasma concentration of TNF alpha, suggesting a pathophysiological role for
TNF alpha in reducing peak peripheral blood flow in CHF.
ORIGINAL PAPERS
Tumour necrosis factor alpha as a predictor of impaired peak leg blood flow in patients with chronic heart failure
Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College, London, UK. s.anker@ic.ac.uk
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
C. Pavoine and F. Pecker Sphingomyelinases: their regulation and roles in cardiovascular pathophysiology Cardiovasc Res, May 1, 2009; 82(2): 175 - 183. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Doehner, A. C. Bunck, M. Rauchhaus, S. von Haehling, F. M. Brunkhorst, M. Cicoira, C. Tschope, P. Ponikowski, R. A. Claus, and S. D. Anker Secretory sphingomyelinase is upregulated in chronic heart failure: a second messenger system of immune activation relates to body composition, muscular functional capacity, and peripheral blood flow Eur. Heart J., April 1, 2007; 28(7): 821 - 828. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Peschel, M. Schonauer, H. Thiele, S. Anker, G. Schuler, and J. Niebauer Invasive assessment of bacterial endotoxin and inflammatory cytokines in patients with acute heart failure Eur J Heart Fail, October 1, 2003; 5(5): 609 - 614. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. F. Singh Exercise Comes of Age: Rationale and Recommendations for a Geriatric Exercise Prescription J. Gerontol. A Biol. Sci. Med. Sci., May 1, 2002; 57(5): M262 - 282. [Full Text] |
||||
![]() |
R Sharma and S.D Anker From tissue wasting to cachexia: changes in peripheral blood flow and skeletal musculature Eur. Heart J. Suppl., April 1, 2002; 4(suppl_D): D12 - D17. [Abstract] [PDF] |
||||
![]() |
D. P. Kotler Cachexia Ann Intern Med, October 17, 2000; 133(8): 622 - 634. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. D. Anker and A. J. S. Coats Cardiac Cachexia: A Syndrome With Impaired Survival and Immune and Neuroendocrine Activation Chest, March 1, 1999; 115(3): 836 - 847. [Abstract] [Full Text] [PDF] |
||||






