title: Low hepatic lipase activity is a novel risk factor for coronary artery disease.
abstract: BACKGROUND
  The crucial function of hepatic lipase (HL) in lipid metabolism has been well established, but the relationship between HL activity and coronary artery disease (CAD) is disputed.
  
  
  RESULTS
  We measured HL activity in the postheparin plasma of 200 consecutive men undergoing elective coronary angiography and determined the degree of CAD with the extent score, which has been shown to be better correlated with known risk factors than other measures of CAD extent. We found a significant inverse correlation between HL activity and the extent of CAD (r=-0.19, P<0.01). This association was mainly due to patients with HDL levels >0.96 mmol/L (n=94, r=-0.30, P<0.005). HL activity was lower in 173 patients with CAD than in 40 controls with normal angiograms (286+/-106 versus 338+/-108 nmol. mL(-1). min(-1), P<0.01). To correct for potential confounding factors, we performed multivariate analyses that confirmed the independent association of HL activity with CAD extent. In addition, the presence of the T allele at position -514 in the HL promoter, which leads to a reduced HL promoter activity, was associated with lower HL activity (r=0.30, P<0.001) and higher CAD extent (42.2+/-20.8 versus 35.3+/-23.6 [extent score], P<0.05). In patients with heterozygous familial hypercholesterolemia, calcified lesions in ECG-gated spiral computed tomography were higher in patients with low HL activity (6.3+/-6.8 versus 1.5+/-3.1, P=0.01).
  
  
  CONCLUSIONS
  Our data show that low HL activity is associated with CAD. Therefore, HL might be useful for CAD risk estimation and might be a target for pharmacological intervention.
authors.affiliation: Department of Internal Medicine I, Internal Medicine III, University of Heidelberg, Heidelberg, Germany. klaus_dugi@med.uni-heidelberg.de
authors.forename: K A
authors.initials: KA
authors.lastname: Dugi
authors.forename: K
authors.initials: K
authors.lastname: Brandauer
authors.forename: N
authors.initials: N
authors.lastname: Schmidt
authors.forename: B
authors.initials: B
authors.lastname: Nau
authors.forename: J G
authors.initials: JG
authors.lastname: Schneider
authors.forename: S
authors.initials: S
authors.lastname: Mentz
authors.forename: T
authors.initials: T
authors.lastname: Keiper
authors.forename: J R
authors.initials: JR
authors.lastname: Schaefer
authors.forename: C
authors.initials: C
authors.lastname: Meissner
authors.forename: H
authors.initials: H
authors.lastname: Kather
authors.forename: M L
authors.initials: ML
authors.lastname: Bahner
authors.forename: W
authors.initials: W
authors.lastname: Fiehn
authors.forename: J
authors.initials: J
authors.lastname: Kreuzer
mesh_terms: D000328:Adult; D000483:Alleles; D003324:Coronary Artery Disease / Q000097:blood / Q000201:enzymology / Q000473:pathology*; D003331:Coronary Vessels / Q000201:enzymology / Q000473:pathology; D006801:Humans; D008049:Lipase / Q000097:blood* / Q000235:genetics; D008099:Liver / Q000201:enzymology*; D008297:Male; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D008049:Lipase