CLINICAL STUDY: HEART FAILURE
Preservation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelial dysfunction
Angus K. Nightingale, MRCP*,
Daniel J. Blackman, MRCP*,
Gethin R. Ellis, MRCP*,
Matthias Schmitt, MRCP*,
Jayne A. Morris-Thurgood, PhD*,
Elizabeth A. Jones, PhD and
Michael P. Frenneaux, MD, FRCP, FESC, FACC*
* Department of Cardiology, University of Wales College of Medicine, Cardiff, United Kingdom
Department of Medical Physics and Clinical Engineering, University Hospital of Wales, Cardiff, United Kingdom
Manuscript received June 21, 2000;
revised manuscript received November 3, 2000,
accepted December 12, 2000.
Reprint requests and correspondence: Professor M. P. Frenneaux, Department of Cardiology, Wales Heart Research Institute, University of Wales College of Medicine, Heath Park, Cardiff CF14 4XN, United Kingdom
OBJECTIVES
The goal of this study was to assess whether endothelial dysfunction occurs in the forearm venous capacitance bed of patients with chronic heart failure (CHF) and to determine the role of nitric oxide (NO) in modulating venous tone.
BACKGROUND
Control of venous tone is crucially important in CHF. More than 70% of blood volume lies in the venous capacitance beds. Therefore, small changes in venous tone may markedly affect cardiac filling pressures and cardiac output.
METHODS
Venous tone was measured using radionuclide forearm venous plethysmography in 24 patients with CHF and 16 age-matched controls. The effect of basal NO activity on venous tone was assessed by infusing N-monomethyl-L-arginine 12 mg/min and stimulated NO using carbachol 15 µg/min. Brachial artery flow-mediated dilation was assessed by ultrasonic wall-tracking.
RESULTS
Blockade of basal NO release caused a significant and similar venoconstriction in patients (9.6 ± 1.8%, p < 0.01) and controls (6.6 ± 1.7%, p < 0.01). Carbachol-induced venodilation was significant and similar in patients (36.8 ± 3.9%, p < 0.001) and controls (40.7 ± 3.9%, p < 0.001). Brachial artery flow-mediated dilation was impaired in patients compared with controls (2.0 ± 0.6% vs. 7.5 ± 2.5%, p < 0.01).
CONCLUSIONS
Our data indicate that, despite marked impairment of the function of the arterial endothelium, there is preservation of both basal and stimulated NO release in the forearm venous capacitance bed. This may provide important insights into mechanisms of endothelial dysfunction in CHF and the potential for novel therapy.
|
Abbreviations and Acronyms
| | ACE | = angiotensin-converting enzyme | | ANOVA | = analysis of variance | | CHF | = chronic heart failure | | FMD | = flow-mediated dilation | | L-NMMA | = N-monomethyl-L-arginine | | NO | = nitric oxide | | NOS | = nitric oxide synthase | | NYHA | = New York Heart Association classification |
|
This article has been cited by other articles:
|
|
|
|
 
E. R. Rabelo, K. Ruschel, H. Moreno Jr., M. Rubira, F. M. Consolim-Colombo, M. C. Irigoyen, and L. E. Rohde
Venous endothelial function in heart failure: Comparison with healthy controls and effect of clinical compensation
Eur J Heart Fail,
August 1, 2008;
10(8):
758 - 764.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Dworakowski, S. Walker, A. Momin, J. Desai, A. El-Gamel, O. Wendler, M. T. Kearney, and A. M. Shah
Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase-Derived Superoxide and Vascular Endothelial Dysfunction in Human Heart Failure
J. Am. Coll. Cardiol.,
April 8, 2008;
51(14):
1349 - 1356.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. R. Maher, A. B. Milsom, P. Gunaruwan, K. Abozguia, I. Ahmed, R. A. Weaver, P. Thomas, H. Ashrafian, G. V.R. Born, P. E. James, et al.
Hypoxic Modulation of Exogenous Nitrite-Induced Vasodilation in Humans
Circulation,
February 5, 2008;
117(5):
670 - 677.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Balmain, N. Padmanabhan, W. R. Ferrell, J. J. Morton, and J. J.V. McMurray
Differences in arterial compliance, microvascular function and venous capacitance between patients with heart failure and either preserved or reduced left ventricular systolic function
Eur J Heart Fail,
September 1, 2007;
9(9):
865 - 871.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. L. Bots, J. Westerink, T. J. Rabelink, and E. J.P. de Koning
Assessment of flow-mediated vasodilatation (FMD) of the brachial artery: effects of technical aspects of the FMD measurement on the FMD response
Eur. Heart J.,
February 2, 2005;
26(4):
363 - 368.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. R. Morgan, L. J. Dixon, C. G. Hanratty, S. M.T. Hughes, W. J. Leahey, K. P. Rooney, G. D. Johnston, and G. E. McVeigh
Impaired endothelium-dependent and -independent vasodilation in elderly patients with chronic heart failure
Eur J Heart Fail,
December 1, 2004;
6(7):
901 - 908.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Schmitt, P. Gunaruwan, N. Payne, J. Taylor, L. Lee, A. J.M. Broadley, A. K. Nightingale, J. R. Cockcroft, A. D. Struthers, J. V. Tyberg, et al.
Effects of Exogenous and Endogenous Natriuretic Peptides on Forearm Vascular Function in Chronic Heart Failure
Arterioscler. Thromb. Vasc. Biol.,
May 1, 2004;
24(5):
911 - 917.
[Abstract]
[Full Text]
|
|
|
|
