title: Serum concentration of insulin-like growth factor-I, but not tumor necrosis factor-alpha, measured twelve months after stenting of the infarct-related artery, is associated with in-stent restenosis.
abstract: Percutaneous coronary intervention (PCI) has revolutionized the management of and outcomes in patients with ST-segment elevation myocardial infarction (STEMI). The role of insulin-like growth factor-I (IGF-I) and tumor necrosis factor-alpha (TNF-alpha) in restenosis has been intensively studied. We aimed to investigate the power of serum IGF-I and TNF-alpha concentrations to predict restenosis in patients who had previously undergone PCI for STEMI. Thirty-seven patients were enrolled in the study. Twelve months prior to the study they underwent successful PCI with stent placement for STEMI. The patients were divided into two groups: group 1 - patients with in-stent restenosis in the infarct-related artery (N=9); group 2 - patients without in-stent restenosis in the infarct-related artery (N=28). Baseline profile was similar in both groups. The mean diameter and length of placed stents were similar in both groups. Smaller minimal lumen diameter (MLD) and greater lumen loss (LL) were observed in group 1. Median IGF-I concentrations were substantially higher in patients with ISR compared to those without ISR (170 ng/mL vs 115 ng/mL, p=0.004). Strikingly, median TNF-alpha levels were lower in group 1 (2.4 pg/mL vs 4.1 pg/mL, p=0.05). Correlation analysis showed that serum IGF-I levels were significantly associated with diameter stenosis (R=0.29 p=0.05), LL (R=0.37 p=0.02), MLD (R= -0.38 p=0.03), and stent length (R=0.30 p=0.05). The cut-off value to predict restenosis for IGF-I was less than 158 ng/mL (sensitivity 55 percent, specificity 93 percent, positive predictive value 71 percent, negative predictive value 87 percent). IGF-I detected twelve months after stent placement during the acute phase of AMI may be a late determinant of restenosis. High concentrations of IGF-I could play a permissive role in the progression of NIH and subsequently restenosis. It seems that as far as TNF-alpha is concerned, diagnostic value remains inconclusive.
authors.affiliation: 3rd Department of Cardiology, Silesian Center for Heart Disease, Silesian Medical University, Zabrze, Poland. bartekh@mp.pl
authors.forename: Janusz
authors.initials: J
authors.lastname: Szkodzinski
authors.forename: B
authors.initials: B
authors.lastname: Hudzik
authors.forename: W
authors.initials: W
authors.lastname: Romanowski
authors.forename: K
authors.initials: K
authors.lastname: Wilczek
authors.forename: A
authors.initials: A
authors.lastname: Danikiewicz
authors.forename: M
authors.initials: M
authors.lastname: Gasior
authors.forename: L
authors.initials: L
authors.lastname: Polonski
authors.forename: B
authors.initials: B
authors.lastname: Zubelewicz-Szkodzinska
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D001772:Blood Cell Count; D023903:Coronary Restenosis / Q000097:blood* / Q000453:epidemiology; D005260:Female; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000601:surgery*; D012372:ROC Curve; D015607:Stents; D013318:Stroke Volume; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I