Association of lipoprotein lipase gene polymorphisms with coronary artery disease

Citation
Jl. Anderson et al., Association of lipoprotein lipase gene polymorphisms with coronary artery disease, J AM COL C, 33(4), 1999, pp. 1013-1020
Citations number
36
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
0735-1097 → ACNP
Volume
33
Issue
4
Year of publication
1999
Pages
1013 - 1020
Database
ISI
SICI code
0735-1097(19990315)33:4<1013:AOLLGP>2.0.ZU;2-W
Abstract
OBJECTIVES The purpose of this study was to test whether the HindIII (+) an d PvuII (-) or (+) restriction enzyme-defined alleles are associated with a ngiographic coronary artery disease (CAD). BACKGROUND Lipoprotein lipase (LPL) plays a central role in lipid metabolis m, hydrolyzing triglyceride in chylomicrons and very low density lipoprotei ns. Polymorphic variants of the LPL gene are common and might affect risk o f CAD. METHODS Blood was drawn from 725 patients undergoing coronary angiography. Leukocyte deoxyribonucleic acid segments containing the genomic sites were amplified by the polymerase chain reaction and digested, and polymorphisms were identified after electrophoresis in 1.5% agarose gel. RESULTS In no-CAD control subjects (n = 168), HindIII (-) and (+) allelic f requencies were 28.6% and 71.4%, and (-) and (+) alleles were carried by 44 .0% and 86.9% of subjects, respectively. Control PvuII (-) and (+) allelic frequencies were 41.7% and 58.3%, and (-) and (+) alleles were carried by 6 4.3% and 81.0%, respectively. In CAD patients (>60% stenosis; n = 483), Hin dIII (+) allelic carriage was increased (93.8% of patients, odds ratio [OR] = 2.25, confidence interval [CI] 1.27 to 4.00). Also, PvuII (-) allelic ca rriage tended to be more frequent in CAD patients (OR = 1.33, CI 0.92 to 1. 93). Adjusted for six CAD risk factors and the other polymorphism, HindIII (+) carriage was associated with an OR = 2.86, CI 1.50 to 5.42, p = 0.0014, and PvuII (-) carriage, OR = 1.42, CI 0.95 to 2.12, p = 0.09. The two poly morphisms were in strong linkage disequilibrium, and a haplotype associatio n was suggested. CONCLUSIONS The common LPL polymorphic allele, HindIII (+), is moderately a ssociated with CAD, and the PvuII (-) allele is modestly associated (trend) . Genetic variants of LPL deserve further evaluation as risk factors for CA D. (J Am Coil Cardiol 1999;33:1013-20) (C) 1999 by the American College of Cardiology.