Antioxidative activity of sulodexide, a glycosaminoglycan, in patients with stable coronary artery disease: a pilot study.
BACKGROUND
Oxidative stress may promote chronic inflammation and contribute to accelerated atherogenesis in patients with coronary artery disease (CAD). Sulodexide, a glycosaminoglycan consisting primarily of heparin, has been shown to affect oxidative stress in experimental settings. The purpose of this pilot study was to determine the effect of sulodexide administration on oxidative stress, inflammation and plasma lipids in patients with proven stable CAD.


METHODS
Fifty-six optimally treated male CAD patients (pts), mean age 57+/-6 yrs, were randomized to either 8 weeks of sulodexide treatment (SUL, n=28), or to a control group (n=28). At baseline and at the end of the study, all pts underwent full clinical and standard laboratory plasma level assessment of lipids, markers of inflammation, and 8-isoprostane, as a sensitive index of oxidative stress.


RESULTS
At entry the 2 groups did not differ significantly in terms of age, coronary risk factors, clinical status and concomitant medication. SUL treatment appeared to be safe and caused a significant decrease in the level of plasma 8-isoprostane (77.4 vs 44.5 pg/ml, p<0.0001) compared with controls (75.7 vs 68.3 pg/ml, p=NS). In contrast, neither LDL cholesterol (2.71 vs 2.72 mmol/l) and triglycerides (1.38 vs 1.43 mmol/l), nor markers of inflammation - fibrinogen (3.7 vs 3.6 g/l), C-reactive protein (0.14 vs 0.13 mg/l), leukocyte count (6.33 vs 6.32x10(9)/l) - were affected by SUL treatment.


CONCLUSIONS
Sulodexide administration resulted in significant reduction in oxidative stress in stable CAD patients, and neither the changes in cholesterol metabolism nor in systemic inflammation underlay this effect.
Bilinska
Maria
M
Department of Cardiac Rehabilitation and Noninvasive Electrocardiology, Institute of Cardiology, Warsaw, Poland. mbilinska@ikard.pl
Wolszakiewicz
Jadwiga
J
Duda
Monika
M
Janas
Jadwiga
J
Beresewicz
Andrzej
A
Piotrowicz
Ryszard
R
D000975:Antioxidants / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005340:Fibrinogen / Q000378:metabolism; D006025:Glycosaminoglycans / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D007958:Leukocyte Count; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects; D010865:Pilot Projects
D000975:Antioxidants; D015415:Biomarkers; D006025:Glycosaminoglycans; D008055:Lipids; C075750:8-epi-prostaglandin F2alpha; C007858:glucuronyl glucosamine glycan sulfate; D005340:Fibrinogen; D002097:C-Reactive Protein; D015237:Dinoprost