Plasma Homocysteine Concentration and Genotype Variation of Enzymes as Risk Factors in Patients with Coronary Artery Disease.
10.4070/kcj.2001.31.8.757
- Author:
Sang Gon KIM
1
;
Young Dae KIM
;
Sung Geun KIM
;
Se Jun JANG
;
Hae Jong CHOI
;
Bong Keun KIM
;
Su Hun LEE
;
Tae Ho PARK
;
Doo Gyung YANG
;
Kwang Soo CHA
;
Moo Hyun KIM
;
Jong Seong KIM
;
Jin Yeong HAN
;
Jung Man KIM
Author Information
1. Division of Cardiology,Dong-A University College of Medicine, Pusan, Korea.
- Publication Type:Original Article
- Keywords:
Homocysteine;
Coronary artery disease;
Methylenetetrahydrofolate reductase;
Cystathionine beta synthase;
Genotype variation
- MeSH:
Coronary Artery Disease*;
Coronary Vessels*;
Cystathionine beta-Synthase;
Cytosine;
Fasting;
Folic Acid;
Genotype*;
Homocysteine*;
Humans;
Linear Models;
Metabolism;
Methylenetetrahydrofolate Reductase (NADPH2);
Obesity;
Oxidoreductases;
Plasma*;
Polymerase Chain Reaction;
Risk Factors*;
Smoke;
Smoking;
Thymidine;
Vitamin B 12
- From:Korean Circulation Journal
2001;31(8):757-766
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Increased plasma homocysteine(tHcy) has been implicated as an independent risk factor for coronary artery diseas(CAD), but the relationship has not been firmly established. Present study aimed to determine the difference of plasma homocysteine between patients with CAD and normal control, and to identify the relation between plasma homocysteine and genotype variation of its metabolic enzymes, and serological characteristics. METHODS: Plasma homocysteine, fasting and post-methionin loading, folate and vitamin B12 were measured among 149 patients and 80 control subjects. Both group consisted of those younger than 65 years. Frequencies of prevalent mutations of enzymes involved in homocysteine metabolism, cytosine to thymidine transition (C(677)T) of methylentetrahydrofolate reductase (MTHFR) was determined by polymerase chain reaction (PCR) in 85 patients and 47 control. RESULT: There was no significant difference in homocysteine level between patients and control group (fasting tHcy; 10.4 +/- 3.6 vs 11.4 +/- 8.4 ng/ml, post-methionine loading tHcy; 18.8 +/- 4.9 vs 17.2 +/- 9.5 ng/ml, p> 0.05 respectively). Genotype frequency of MTHFR C(677)T was similar between two groups. Plasma homocysteine level did not appear to vary with genotypes of MTHFR both in patients and control subjects. Multiple linear regression analysis identified smoking as the most significant factor affecting plasma homocysteine level, followed by age, MTHFR genotype, obesity, and folate level. CONCLUSION: Homocysteine concentration was not different between controls and patients with CAD. Significant variation of homocysteine level according to genetypic polymorphism of metabolism enzymes was not observed. On multiple linear regression, several factors were identified to be related to homocysteine level, including MTHFR genotype. Further study is warranted to clarify the significance of homocysteine in the development of CAD.
