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1.
Chinese Journal of Medical Genetics ; (6): 233-235, 2008.
Article in Chinese | WPRIM | ID: wpr-229782

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the association of the 4G/5G polymorphism located in the promoter region of plasminogen activator inhibitor-1(PAI-1) gene with prognosis of coronary artery disease (CAD) in Chinese Hans.</p><p><b>METHODS</b>One hundred and fifty five patients with CAD and 190 unrelated healthy control individuals were included in the study. The 4G/5G polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis. A follow-up survey of major adverse cardiovascular event (MACE) and analysis of the relationship between the severity of coronary vessels and PAI-1 gene polymorphism were carried out.</p><p><b>RESULTS</b>(1) The frequency of 4G/4G genotype of PAI-1 gene was higher in CAD patients than in controls (58/155, 37.42% vs 52/190, 27.37%, P< 0.01). (2) The frequency of 4G/4G genotype of PAI-1 in patients with MACE was higher than that in patients without MACE (40/81, 49.38% vs 18/74, 23.42%; P< 0.01). (3) The frequency of 4G/4G genotype in patients with multivessel disease was higher than that in patients with single-vessel disease (30/47, 44.77% vs 9/37, 24.32%; P< 0.05).</p><p><b>CONCLUSION</b>The 4G/5G polymorphism located in the promoter region of PAI-1 gene was associated with prognosis of CAD patients, and may be regarded as a biomarker of the severity of the involved vessels.</p>


Subject(s)
Female , Humans , Male , Coronary Artery Disease , Genetics , Gene Frequency , Genetic Predisposition to Disease , Genetics , Genotype , Plasminogen Activator Inhibitor 1 , Genetics , Polymorphism, Genetic , Genetics
2.
Chinese Journal of Cardiology ; (12): 1024-1028, 2007.
Article in Chinese | WPRIM | ID: wpr-299535

ABSTRACT

<p><b>OBJECTIVE</b>To observe the association between angiotensin-converting enzyme (ACE) gene polymorphism and endothelial nitric oxide synthase (eNOS) gene polymorphism and risk of coronary artery disease (CAD) in Han Chinese.</p><p><b>METHODS</b>The polymorphism in the ACE and eNOS gene were detected by using polymerase chain reaction-restriction fragment length polymorphism analysis, blood pressure (BP), blood lipids, blood glucose (BS), body mass index (BMI) and left ventricle eject fraction (LVEF) were determined 236 patients with CAD and 190 healthy individuals.</p><p><b>RESULTS</b>The frequencies of DD genotype of ACE were higher and the II genotype were lower in CAD patients than in controls (P < 0.05). CAD patients with DD genotypes were related with higher serum TG, lower HDL-C, higher BS levels, higher BWI and lower LVEF compared to CAD patients with II and ID genotypes of ACE (all P < 0.05), while SBP, DBP, TC and LDL-C levels were similar among CAD patients and controls with different genotypes of ACE (P > 0.05). The genotype distributions of ACE and eNOS were also similar among CAD patients with or without diabetes mellitus/ACS, with single or multiple vessel diseases (P > 0.05). The frequency of GT genotype of eNOS was higher in CAD patients than in controls (P < 0.01) while the frequency of GG genotype in CAD patients and controls was similar (P > 0.05) and eNOS genotypes were not related to TC, TG, HDL-C, LDL-C, BS, BMI, SBP, DBP and LVEF levels among CAD patients and controls (P > 0.05). The risk of suffering from CAD in population with ACE DD genotype is 1.74 times higher than that with II genotype (P < 0.01) and 1.73 times higher in population with eNOS GT genotype than that with GT genotype (P < 0.05). The risk of suffering from CAD is 37.9% with II and GG genotypes and 77.8% with DD and GT genotypes.</p><p><b>CONCLUSION</b>The ACE and eNOS genotype polymorphisms were associated with risk of CAD and persons with DD and GT genotypes take higher risk of suffering from CAD.</p>


Subject(s)
Aged , Female , Humans , Male , Middle Aged , Case-Control Studies , Coronary Artery Disease , Genetics , Gene Frequency , Genotype , Nitric Oxide Synthase Type III , Genetics , Peptidyl-Dipeptidase A , Genetics , Polymorphism, Single Nucleotide
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