The ACE gene D/I polymorphism did not predict coronary in-stent restenosis overall (p=NS), but restenosis was higher in DD genotype patients treated with ACE inhibitors (40% vs 12%, p=0.006).
Cohort (n=369)
Does the ACE gene D/I polymorphism predict coronary in-stent restenosis in patients undergoing stent implantation?
The ACE gene D/I polymorphism is not an independent predictor of in-stent restenosis overall, but the DD genotype may increase restenosis risk in patients treated with ACE inhibitors or ARBs.
Absolute Event Rate: 15.7% vs 16.4%
p-value: p=NS
OBJECTIVES: This study aimed to clarify the role of the angiotensin-converting enzyme (ACE) gene polymorphism in the development of in-stent restenosis. BACKGROUND: In-stent restenosis occurs after treatment of coronary artery stenosis in 12% to 32% of coronary interventions with stents. Experimental and clinical studies have suggested that the deletion/insertion (D/I) polymorphism of the ACE gene plays a role in this. METHODS: Quantitative coronary angiography before, immediately after and six months after stent implantation were compared in 369 patients, in whom D/I typing of the ACE gene was performed. RESULTS: At follow-up we found no differences between the three genotypes in minimal lumen diameter (homozygotes with two deletion alleles in the ACE gene DD, 2.20 mm; heterozygotes with one deletion and one insertion allele in the ACE gene DI, 2.19 mm; and homozygotes with two insertion alleles in the ACE gene II, 2.25 mm). The corresponding diameter stenoses were: DD: 25%, DI: 27%, II: 27% (p = NS), and the frequency of restenosis (>50% diameter stenosis) was: DD: 15.7%, DI: 11.0% and II: 16.4% (p = NS). Logistic regression analysis identified diabetes (odds ratio OR: 3.0, 95% confidence interval CI: 1.0 to 8.7), lesion length (OR: 1.1, 95% CI: 1.01 to 1.30) and minimal lumen diameter immediately after the intervention (OR: 0.3, 95% CI: 0.14 to 0.85) as predictors of in-stent restenosis. In a post hoc analysis of patients treated versus those not treated with an ACE-inhibitor antagonist or an angiotensin receptor antagonist, we found an increased frequency of in-stent restenosis in the DD genotypes (40% vs. 12%, p = 0.006). CONCLUSIONS: The D/I polymorphism is not an independent predictor of coronary in-stent restenosis in general, but it may be of clinical importance in patients treated with ACE inhibitors or angiotensin receptor antagonists.
Jørgensen et al. (Thu,) conducted a cohort in Coronary in-stent restenosis (n=369). ACE gene D/I polymorphism vs. Other genotypes (DI, II) was evaluated on Frequency of restenosis (>50% diameter stenosis) (p=NS). The ACE gene D/I polymorphism did not predict coronary in-stent restenosis overall (p=NS), but restenosis was higher in DD genotype patients treated with ACE inhibitors (40% vs 12%, p=0.006).