Abstract
Coronary heart disease (CHD) has been considered as a multifactorial disorder
with the involvement of both environmental and genetic factors. The advent of
tools to investigate individual variability of DNA has allowed us to perform the
association studies of candidate genes. However, an association between genetic
trait and phenotypic variations is not easy to demonstrate and several reported
association between genetic markers and risk factors or overt CHD have gone
unconfirmed. It should not be assumed that for a given genetic trait, the impact
on risk will be similar in all populations. In particular, most studies of the
molecular bases of CHD have involved Caucasian subjects, so much more work with
the Korean population is needed before genetic testing for susceptibility to CHD
can be offered to Koreans as a clinical service. In this review, we discuss two
aspects of the molecular bases of CHD: i) Molecular bases of the candidate gene
related to lipoprotein metabolism including apolipoprotein AI-CIII-AIV gene
duster, apolipoprotein B, apolipoprotein E-CI-CII gene cluster,
apolipoprotein(a), LDL receptors, lipoprotein lipase, cholesteryl ester transfer
protein, and apo B editing protein; ii) Molecular bases of the candidate gene
related to thrombotic and other factors including fibrinogen, factor VII,
plasminogen activator inhibitor 1, homocysteine, stromelysin, paraoxonase, and
angiotensin converting enzyme. Studies involving the Korean population,
especially those performed by our teams, are also summarized.