Stromelysin Gene Promoter 5A/6A Polymorphism and Risk of Restenosis after Coronary Angioplasty
Kee-Hyoung LEE; In-Ho CHAE; Hyun-Jai CHO; Soo-Yeon CHOI; Jae-Ran JU; Seong-Hoon PARK; Dae-Won SOHN; Byung-Hee OH; Myoung-Mook LEE; Young-Bae PARK; Yun-Shik CHOI; Young-Woo LEE.
Korean Circulation Journal
; : 955-960, 2001.
Artículo
en Ko
| WPRIM | ID: wpr-178583
BACKGROUND:
Remodeling of extracellular matrix is one of the main mechanism of restenosis that is the major limitation of percutaneous coronary angioplasty. Stromelysin is one of the matrix metalloproteinase, which catalyze extracellular matrix of the diseased vessels. We studied the effect of 5A/6A stromelysin promotor gene polymorphism on the restenosis after coronary angioplasty. MATERIALS ANDMETHODS:
A total of 64 patients who underwent coronary angioplasty and 6-month follow-up angiogram were enrolled into 4 groups classified by the presence of intracoronary stenting during angioplasty and restenosis in the follow-up angiogram. We analyzed basic clinical data and risk factors for coronary artery disease of all patients. The 5A/6A stromelysin promotor gene polymorphism was analyzed by direct sequencing of polymerase chain reaction products from patient's DNA.RESULTS:
We studied clinical data and stromelysin genotype of 51 feasible patients. We found no significant differences of clinical risk factors between the patients with or without restenosis. The allele frequencies of 5A and 6A were 17% and 83% in total study population, 26% and 74% in patient group without restenosis, 6% and 94% in patients with restenosis, respectively. The frequencies of non6A/6A containing 5A allele(5A/5A and 5A/6A) and 6A/6A was 41% and 59% in non-restenotic group and 12.5% and 87.5% in restenotic group. So the relative risk of restenosis for 6A/6A compared to non6A/6A was 4.83(95% CI 1.15~20.17, p=0.03).CONCLUSION:
Our study for stromelysin 5A/6A polymorphism reveals predominance of 6A allele in Korean patients with coronary artery disease. We conclude that 6A/6A homozygote is the possible genetic risk factor for restenosis after percutaneous coronary angioplasty.
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