Int J Angiol 1993; 2(2): 89-96
DOI: 10.1007/BF02651565
Original Articles

© Georg Thieme Verlag KG Stuttgart · New York

Impairment of endothelium-dependent and endothelium-independent peripheral vasodilation in patients with chronic heart failure due to nonischemic heart disease

Motoyuki Nakamura, Tsutomu Funakoshi, Makoto Chiba, Shinji Makita, Naoshi Arakawa, Katsuhiko Hiramori
  • The Second Department of Internal Medicine, Iwate Medical University, Morioka, Iwate, Japan
Further Information

Publication History

Publication Date:
22 April 2011 (online)


The authors have examined changes in forearm blood flow during local intra-arterial infusion of acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in patients with heart failure due to nonischemic heart disease. Incremental step-up doses of acetylcholine and nitroprusside were infused locally into the brachial artery in 10 healthy controls (group 1), 13 patients with no history of decompensated congestive heart failure (group 2), and 13 patients who exhibited congestive heart failure before admission (group 3). Forearm blood flow was measured by venous occlusion plethysmography.

Systemic blood pressure and heart rate were not affected significantly by either infusion in any of the three groups. Groups 1 and 2 showed similar changes in forearm blood flow after endothelium-dependent and endothelium-independent vasodilation, but these changes were attenuated significantly in group 3 (both p<0.05). Although there were no significant differences in clinical characteristics including hemodynamic parameters between groups 2 and 3, plasma noradrenaline concentration was elevated in group 3 (p<0.01). A significant negative correlation was found between plasma noradrenaline level and nitroprusside- or acetylcholine-induced change in forearm blood flow (nitroprusside: r=−0.36, p<0.05; acetylcholine: r=−0.42, p<0.05). These observations demonstrate that the attenuation of the response to vasodilatory stimuli in the peripheral vasculature may persist in the convalescent phase after decompensated heart failure and that the vascular dysfunction may be due not only to endothelial dysfunction but also to an endothelium-independent mechanism such as neurohormonal activation.