Association of Angiotensin-Converting Enzyme Gene Polymorphism and Angiotensin-Converting Enzyme Activity in Korean patients with Coronary Artery Disease.
10.4070/kcj.2000.30.11.1350
- Author:
Sung Uk KWON
;
Duk Kyung KIM
;
Ji Hyang KIM
;
Joong Il PARK
;
Mi Hyang KOAK
;
Ju Hyeon OH
;
Jin Ok JEONG
;
Sang Chol LEE
;
Hyeon Cheol GWON
;
Seung Woo PARK
;
June Soo KIM
;
Sang Hoon LEE
;
Kyung Pyo HONG
;
Jeong Euy PARK
;
Jung Don SEO
;
Won Ro LEE
- Publication Type:Original Article
- MeSH:
Acute Coronary Syndrome;
Angina, Stable;
Angiography;
Apolipoproteins B;
Body Mass Index;
Coronary Angiography;
Coronary Artery Disease*;
Coronary Vessels*;
Gene Frequency;
Genotype;
Humans;
Peptidyl-Dipeptidase A;
Plasma;
Risk Factors
- From:Korean Circulation Journal
2000;30(11):1350-1356
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Insertion/Deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene has been postulated as a risk factor for coronary artery disease. However, controversies exist whether deletion polymorphism in the ACE gene and/or high levels of ACE activity may be a risk factor for coronary artery disease (CAD). We investigated the association of the I/D polymorphism of the ACE gene and serum ACE activity in Korean patients with CAD. METHODS: Study subjects were 629 patients who underwent coronary angiography. CAD group (n=77) was subdivided according to either clinical manifestation or the number of diseased vessels on angiography. The control group comprised 152 patients who did not have a significant coronary lesion. Low risk group (n=5) was defined as subjects with age <55 years, a body mass index (BMI) <26 kg/m2 and a plasma ApoB <125 mg/dl. RESULTS: 1) The genotype and allele frequencies of ACE gene polymorphism were not different between control (DD:DI:II=.20:0.48:0.32, D:I=.44:0.56) and CAD group (DD:DI:II=.18:0.46:0.36, D:I=.41:0.59). 2) When the CAD group was subdivided into stable angina (SA) and acute coronary syndrome (ACS) group, neither ACE genotype nor allele frequencies differed between the SA and ACS group. 3) There was no significant association between the ACE polymorphism and the severity of CAD, as assessed by the number of diseased coronary vessels. 4) A significant difference in serum ACE activity was apparent among ACE genotypes in both controls and CAD subjects. Serum ACE activity in individuals with the DD genotype was significantly greater than that in individuals with DI or II genotypes. 5) There was no difference in serum ACE activity between controls and the CAD subjects of all genotypes or of the same genotype. 6) There was no association between the ACE polymorphism or serum AC activity and CAD in the low risk group. CONCLUSIONS: We have shown that neither the ACE I/D polymorphism nor serum ACE activity act as an independent risk factor in the development of CAD in Korean. This result indicates that the gene polymorphism and variation in serum ACE activity are not risk factors for CAD in this population.
