Presentation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelialdysfunction
Ak. Nightingale et al., Presentation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelialdysfunction, J AM COL C, 37(4), 2001, pp. 1062-1068
Citations number
41
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
OBJECTIVES The goal of this study was to assess whether endothelial dysfunc
tion occurs in the forearm venous capacitance bed of patients with chronic
heart failure (CHF) and to determine the role of nitric oxide (NO) in modul
ating venous tone.
BACKGROUND Control of venous tone is crucially important in CHF. More than
70% of blood volume lies in thr venous capacitance beds. Therefore, small c
hanges in venous tone may markedly affect cardiac filling pressures and car
diac output.
METHODS Venous tone was measured using radionuclide forearm venous plethysm
ography 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-ar
ginine 12 mg/min and stimulated NO using carbachol 15 mug/min. Brachial art
ery flow-mediated dilation was assessed by ultrasonic wall-tracking.
RESULTS Blockade of basal NO release caused a significant and similar venoc
onstriction in patients (9.6 +/- 1.8%, p < 0.01) and controls (6.6 <plus/mi
nus> 1.7%, p < 0.01). Carbachol-induced venodilation was significant and si
milar in patients (36.8 <plus/minus> 3.9%, p < 0.001) and controls (40.7 <p
lus/minus> 3.9%, p < 0.001). Brachial artery flow-mediated dilation was imp
aired in patients compared with controls (2.0 <plus/minus> 0.6% vs. 7.5 +/-
2.5%, p < 0.01).
CONCLUSIONS Our data indicate that, despite marked impairment uf the functi
on of the arterial endothelium, there is preservation of both basal and sti
mulated NO release in the forearm venous capacitance bed. This may provide
important insights into mechanisms of endothelial dysfunction in CHF and th
r potential for novel therapy. (J Am Coll Cardiol 2001;37:1062-8) (C) 2001
by the American College of Cardiology.