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.

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.

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.

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.