THE PARAOXONASE GLN-ARG-192 POLYMORPHISM IN SUBJECTS WITH ISCHEMIC-HEART-DISEASE

Citation
Gi. Rice et al., THE PARAOXONASE GLN-ARG-192 POLYMORPHISM IN SUBJECTS WITH ISCHEMIC-HEART-DISEASE, Coronary artery disease, 8(11-12), 1997, pp. 677-682
Citations number
34
Journal title
ISSN journal
09546928
Volume
8
Issue
11-12
Year of publication
1997
Pages
677 - 682
Database
ISI
SICI code
0954-6928(1997)8:11-12<677:TPGPIS>2.0.ZU;2-V
Abstract
Background Human serum paraoxonase activity is related to the paraoxon ase Gln-Arg 192 polymorphism genotype. The purpose of this study was t o investigate the association between the Gln-Arg 192 polymorphism of paraoxonase and ischaemic heart disease (IHD). Methods Four hundred an d forty patients with a history suggestive of IHD, and characterized b y coronary angiography, and 527 healthy controls were studied. Patient s were grouped according to paraoxonase genotype, presence or absence of diseased coronary arteries (on the basis of 50% stenosis), and hist ory of myocardial infarction as judged by World Health Organization cr iteria. Patients were genotyped for the paraoxonase Gln-Arg 192 polymo rphism by polymerase chain reaction. Results No significant relationsh ip was found between paraoxonase genotype and age, sex, body mass inde x, smoking, triglycerides or hypertension. However, by one-way analysi s of variance, cholesterol was found to be significantly associated wi th paraoxonase genotype in male patients [AA 5.9 (5.8-6.1), AB 6.2 (6. 0-6.4), BB 5.7 (5.4-6.1); P = 0.04]. The Gln-Arg 192 polymorphism was found to have no significant effect on the number of patients having d iseased coronary arteries, or having myocardial infarction (P = 0.97 f or both). In logistic regression models, paraoxonase genotype did not remain a significant independent predictor of stenosis or myocardial i nfarction. Conclusion This study failed to show an association between the Gln-Arg 192 polymorphism of paraoxonase and the clinical phenotyp es of coronary atheroma and acute myocardial infarction.