Korean J Med.
2000 Apr;58(4):402-410.
Effect of angiotensin converting enzyme and nitric oxide synthase polymorphisms and the effect of interaction between the polymorphisms on the restensois after coronary angioplasty in Korea
- Affiliations
-
- 1Department of Internal Medicine, College of Medicine, Seoul National University.
- 2Department of Medicine, College of Medicine, Hallym University.
- 3Cardiovascular Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea.
Abstract
- BACKGROUND
Intimal hyperplasia and vascular remodeling are major mechanisms of restenosis
after coronary artery angioplasty. Angiotensin II causes restenosis by stimulating cell proliferation
and vascular constriction and nitric oxide prevents restenosis by inhibiting cell proliferation and
stimulating vascular dilatation. Angiotensin converting enzyme (ACE) and nitric oxide synthase (NOS)
are the main determinants of the activity of the angiotensin II and the nitric oxide. In this study,
we tested whether the genetic polymorphisms of the ACE and the NOS gene are the risk factors of restenosis
and whether the effect of the genetic polymorphisms in stent group is different from that in balloon
angioplasty group. We also tested whether there are interactions among the polymorphisms.
METHODS
We determined ACE I/D polymorphism and NOS A/B and G/T polymorphism in 219patients (77 patients
(81 lesions) in stent group and 142 patients (181 lesions) in balloon angioplasty group) who underwent
PTCA and follow up coronary angiography in Seoul national university hospital from January 1996 to May
1999.
RESULTS
Restenosis (50% of reference diameter) was observed in 78/262(30%) lesions (18/81(22%)
lesions in stent group, 60/181(33%) lesions in balloon angioplasty group). ACE DD genotype is the significant
risk factor for increment of late luminal loss and loss index in stent group. In stent group, means of
the late luminal loss and loss index of the lesions of the DD genotype are 1.12+/-0.61mm and 74.7+/-38.3%
and those of the non-DD genotype are 0.72+/-0.77mm and 44.9+/-67.5% but DD genotype is not the risk factor
for restenosis after balloon angioplasty. The restenosis rate, late luminal loss and loss index are not
significantly different according to NOS polymorphisms. No significant interaction among the polymorphisms
is observed.
CONCLUSION
ACE DD genotype is a significant risk factor for restenosis after stent insertion
but is not a risk factor for restenosis after balloon angioplasty in Korean. This result reflects the different
mechanism of restenosis after stent insertion and balloon angioplasty. NOS polymorphisms are not associated
with restenosis and no interaction between the polymorphisms is observed.