title: The prediction of coronary artery disease based on non-invasive examinations and heme oxygenase 1 polymorphism versus virtual histology.
abstract: OBJECTIVE
  Prediction of coronary atherosclerosis in patients with stable angina based on non-invasive examinations.
  
  
  METHODS
  Pro-inflammatory markers, heme oxygenase-1 (HO-1) polymorphism, lipid levels, Framingham risk score (FRS), and carotid ultrasound were analyzed and compared to grayscale and virtual histology intravascular ultrasound (VH-IVUS).
  
  
  RESULTS
  A total of 101 patients were included, and genetic analysis was performed on 81 patients (80.2%). The HO-1 risk polymorphism was more frequent in patients post-myocardial infarction (61.3% vs 32%; P=.0097), or with diabetes (68.4% vs 35.5%; P=.011) or a higher FRS (21.5 vs 15.7; P=.014). Plaques in patients with the HO-1 risk polymorphism contained less fibro-fatty tissue (17.1% vs 23.2%; P=.005) and more necrotic core (NC; 17.1% vs 12.7%; P=.02) and calcification (10.2% vs 5.7%; P=.035) compared to patients without the HO-1 risk polymorphism. Carotid intima media thickness (P=.05) and carotid bulb plaque (P=.008) predicted plaque burden. The level of Apo A inversely correlated with NC (P=.047; r = -0.27) and was lower in patients with VH-thin-cap fibroatheroma (VH-TCFA; 1.19 mmol/L vs 1.3 mmol/L; P=.04). FRS correlated with NC (P=.007; r = 0.2), with angiographic disease severity (P=.032; r = 0.21) and was higher in patients with VH-TCFA (9.1 vs 7.8; P=.03).
  
  
  CONCLUSIONS
  Carotid ultrasound and HO-1 polymorphism improve coronary atherosclerosis prediction.
authors.affiliation: 2nd Department of Medicine - Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, II. interni klinika, U nemocnice 2, Prague, 12808 Czech Republic. tomas.kovarnik@vfn.cz
authors.forename: Tomas
authors.initials: T
authors.lastname: Kovarnik
authors.forename: Ales
authors.initials: A
authors.lastname: Kral
authors.forename: Hana
authors.initials: H
authors.lastname: Skalicka
authors.forename: Gary S
authors.initials: GS
authors.lastname: Mintz
authors.forename: Lubomir
authors.initials: L
authors.lastname: Kralik
authors.forename: Martin
authors.initials: M
authors.lastname: Chval
authors.forename: Jan
authors.initials: J
authors.lastname: Horak
authors.forename: Lenka
authors.initials: L
authors.lastname: Skalicka
authors.forename: Milan
authors.initials: M
authors.lastname: Sonka
authors.forename: Andreas
authors.initials: A
authors.lastname: Wahle
authors.forename: Richard W
authors.initials: RW
authors.lastname: Downe
authors.forename: Jana
authors.initials: J
authors.lastname: Uhrova
authors.forename: Hana
authors.initials: H
authors.lastname: Benakova
authors.forename: Lenka
authors.initials: L
authors.lastname: Cernohousova
authors.forename: Pavel
authors.initials: P
authors.lastname: Martasek
authors.forename: Jan
authors.initials: J
authors.lastname: Belohlavek
authors.forename: Michael
authors.initials: M
authors.lastname: Aschermann
authors.forename: Ales
authors.initials: A
authors.lastname: Linhart
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000175:diagnosis / Q000235:genetics / Q000473:pathology; D001054:Apolipoproteins A / Q000097:blood; D015415:Biomarkers; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging*; D059168:Carotid Intima-Media Thickness; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D051547:Heme Oxygenase-1 / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010808:Physical Examination; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D012307:Risk Factors
chemical_list: D001054:Apolipoproteins A; D015415:Biomarkers; C496541:HMOX1 protein, human; D051547:Heme Oxygenase-1