Endothelial dysfunction has been described in patients with coronary artery disease (CAD) or chronic heart failure (CHF). Vitamin C administration leads to an improvement of endothelial function by reducing elevated levels of reactive oxygen species. It remains unclear, however, whether the degree of endothelial dysfunction caused by oxidative stress differs between CAD and CHF because of ischemic (ICM) or dilated cardiomyopathy (DCM).

In patients with CAD (n = 9; left ventricular ejection fraction [LVEF], 64% ± 3%), ICM (n = 9; LVEF, 25% ± 4%), DCM (n = 9; LVEF, 25% ± 3%), and healthy subjects (HS; n = 5; LVEF, 66% ± 5%) a change in internal radial artery diameter in response to acetylcholine (Ach; 15 and 30 μg/min) was measured with high-resolution ultrasound scanning during a co-infusion of normal saline or vitamin C (25 mg/min).

Ach-mediated vasodilation was blunted in patients with CHF (DCM, 90 ± 20 μm; ICM, 86 ± 20 μm) and patients with CAD (336 ± 20 μm) as compared with HS (496 ± 43 μm; P <.05 vs patients with DCM, ICM, CAD). Vitamin C co-infusion increased Ach-mediated vasodilation by 180 ± 35 μm (to 270 ± 30 μm) in DCM (P <.05 vs CAD, HS) and by 294 ± 40 μm (to 380 ± 20 μm) in ICM (P <.05 vs DCM, CAD, HS). In patients with CAD, vitamin C increased Ach-mediated vasodilation by 146 ± 35 μm to normal values, whereas vascular diameter remained unchanged in HS (14 ± 20 μm; P = not significant).

Acute vitamin C administration restored peripheral endothelial function in patients with CAD to normal values, whereas endothelial function remained attenuated in CHF, in particular in patients with DCM. These results suggest that in patients with CHF, factors other than oxidative stress (eg, cytokines) contribute to the pathologic endothelial function.