title: Reduction of C-reactive protein with isoflavone supplement reverses endothelial dysfunction in patients with ischaemic stroke.
abstract: OBJECTIVE
  To investigate the effect of oral isoflavone supplement on vascular endothelial function in patients with established cardiovascular disease.
  
  
  RESULTS
  A randomized, double-blinded, placebo-controlled trial was performed to determine the effects of isoflavone supplement (80 mg/day, n = 50) vs. placebo (n = 52) for 12 weeks on brachial flow-mediated dilatation (FMD) in patients with prior ischaemic stroke. Compared with controls, FMD at 12 weeks was significantly greater in isoflavone-treated patients [treatment effect 1.0%, 95% confidence interval (95% CI) 0.1-2.0, P = 0.035]. Adjusted for baseline differences in FMD, isoflavone treatment was independently associated with significantly less impairment of FMD at 12 weeks (odds ratio 0.32, 95% CI 0.13-0.80, P = 0.014). The absolute treatment effect of isoflavone on brachial FMD was inversely related to baseline FMD (r = -0.51, P < 0.001), suggesting that vasoprotective effect of isoflavone was more pronounced in patients with more severe endothelial dysfunction. Moreover, isoflavone treatment for 12 weeks resulted in a significant decrease in serum high-sensitivity (hs)-C-reactive protein level (treatment effect -1.7 mg/L, 95% CI -3.3 to -0.1, P = 0.033). Nevertheless, isoflavone did not have any significant treatment effects on nitroglycerin-mediated dilatation, blood pressure, heart rate, serum levels of fasting glucose and insulin, haemoglobin A1c, and oxidative stress as determined by serum superoxide dismutase, 8-isoprostane, and malondialdehyde (all P > 0.05).
  
  
  CONCLUSIONS
  This study demonstrated that 12 week isoflavone treatment reduced serum hs-C-reactive protein and improved brachial FMD in patients with clinically manifest atherosclerosis, thus reversing their endothelial dysfunction status. These findings may have important implication for the use of isoflavone for secondary prevention in patients with cardiovascular disease, on top of conventional interventions.
authors.affiliation: Cardiology Division, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, PR China.
authors.forename: Yap-Hang
authors.initials: YH
authors.lastname: Chan
authors.forename: Kui-Kai
authors.initials: KK
authors.lastname: Lau
authors.forename: Kai-Hang
authors.initials: KH
authors.lastname: Yiu
authors.forename: Sheung-Wai
authors.initials: SW
authors.lastname: Li
authors.forename: Hiu-Ting
authors.initials: HT
authors.lastname: Chan
authors.forename: Daniel Yee-Tak
authors.initials: DY
authors.lastname: Fong
authors.forename: Sidney
authors.initials: S
authors.lastname: Tam
authors.forename: Chu-Pak
authors.initials: CP
authors.lastname: Lau
authors.forename: Hung-Fat
authors.initials: HF
authors.lastname: Tse
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000188:drug therapy / Q000503:physiopathology; D001916:Brachial Artery / Q000187:drug effects* / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects*; D005260:Female; D006801:Humans; D007529:Isoflavones / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D010919:Placebos; D030262:Soybean Proteins / Q000627:therapeutic use*; D020521:Stroke / Q000188:drug therapy* / Q000503:physiopathology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D007529:Isoflavones; D010919:Placebos; D030262:Soybean Proteins; D002097:C-Reactive Protein