Depletion of antioxidants is associated with no-reflow phenomenon in acute myocardial infarction.
BACKGROUND
No-reflow phenomenon is observed in approximately one-third of patients after percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI), and is associated with poor functional and clinical outcomes. On the other hand, the formation of free radicals in vasculature exerts deleterious effects on coronary microcirculation.


OBJECTIVE
We hypothesized that redox state in coronary circulation may play a crucial role in no-reflow phenomenon in AMI.


METHODS
Consecutive 26 patients with first AMI who underwent primary PCI < 24 h after onset were enrolled. Before PCI, blood samples were obtained from coronary sinus to measure plasma or serum antioxidative vitamins (vitamin C, vitamin E, and beta-carotene) and antioxidative enzymes (extracellular glutathione peroxidase [GPX], superoxide dismutase, and catalase). After PCI, the corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC) was measured in the target vessel. Patients with TIMI < or = 2 flow despite an optimal PCI result were designated as no-reflow group (Group NR, n = 6) and the others as reflow group (Group R, n = 20).


RESULTS
Levels of vitamin C, vitamin E, and GPX before PCI were significantly lower in Group NR than in Group R. The CTFC correlated inversely with levels of vitamin C, vitamin E, and GPX (p < 0.05).


CONCLUSIONS
Depletion of antioxidants is associated with no-reflow phenomenon in AMI. These findings strongly suggest that the redox state in coronary circulation plays an important role in the pathogenesis of no-reflow phenomenon.
Matsumoto
Hidenari
H
Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Inoue
Nobutaka
N
Takaoka
Hideyuki
H
Hata
Katsuya
K
Shinke
Toshiro
T
Yoshikawa
Ryohei
R
Masai
Hiroyuki
H
Watanabe
Satoshi
S
Ozawa
Toru
T
Yokoyama
Mitsuhiro
M
D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000097:blood*; D002374:Catalase / Q000097:blood; D003326:Coronary Circulation / Q000502:physiology*; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D015425:Myocardial Reperfusion; D010084:Oxidation-Reduction; D018709:Statistics, Nonparametric; D013482:Superoxide Dismutase / Q000097:blood; D014810:Vitamin E / Q000097:blood*; D019207:beta Carotene / Q000097:blood
D000975:Antioxidants; D019207:beta Carotene; D014810:Vitamin E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid