title: Improvement of peripheral endothelial dysfunction by acute vitamin C application: different effects in patients with coronary artery disease, ischemic, and dilated cardiomyopathy.
abstract: BACKGROUND
  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).
  
  
  METHODS
  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 microg/min) was measured with high-resolution ultrasound scanning during a co-infusion of normal saline or vitamin C (25 mg/min).
  
  
  RESULTS
  Ach-mediated vasodilation was blunted in patients with CHF (DCM, 90 +/- 20 microm; ICM, 86 +/- 20 microm) and patients with CAD (336 +/- 20 microm) as compared with HS (496 +/- 43 microm; P <.05 vs patients with DCM, ICM, CAD). Vitamin C co-infusion increased Ach-mediated vasodilation by 180 +/- 35 microm (to 270 +/- 30 microm) in DCM (P <.05 vs CAD, HS) and by 294 +/- 40 microm (to 380 +/- 20 microm) in ICM (P <.05 vs DCM, CAD, HS). In patients with CAD, vitamin C increased Ach-mediated vasodilation by 146 +/- 35 microm to normal values, whereas vascular diameter remained unchanged in HS (14 +/- 20 microm; P = not significant).
  
  
  CONCLUSIONS
  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.
authors.affiliation: University of Leipzig, Heart Center, Department of Internal Medicine/Cardiology, Leipzig, Germany.
authors.forename: Sandra
authors.initials: S
authors.lastname: Erbs
authors.forename: Stephan
authors.initials: S
authors.lastname: Gielen
authors.forename: Axel
authors.initials: A
authors.lastname: Linke
authors.forename: Sven
authors.initials: S
authors.lastname: Möbius-Winkler
authors.forename: Volker
authors.initials: V
authors.lastname: Adams
authors.forename: Yves
authors.initials: Y
authors.lastname: Baither
authors.forename: Gerhard
authors.initials: G
authors.lastname: Schuler
authors.forename: Rainer
authors.initials: R
authors.lastname: Hambrecht
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000368:Aged; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D002311:Cardiomyopathy, Dilated / Q000150:complications; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D004359:Drug Therapy, Combination; D004730:Endothelium, Vascular / Q000187:drug effects*; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications; D009599:Nitroprusside / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D000109:Acetylcholine; D001205:Ascorbic Acid