Key result
The ACE DD genotype or D allele was not associated with a higher risk of restenosis at 6 months after coronary stent placement compared to II or ID genotypes (31.2% vs 32.8% and 34.0%; P=0.62).
Why the study?
Does the ACE gene D allele increase the risk of restenosis in patients with coronary artery disease undergoing intracoronary stent implantation?
Cohort (n=1,850)
Does the ACE gene D allele increase the risk of restenosis in patients with coronary artery disease undergoing intracoronary stent implantation?
Absolute Event Rate: 31.2% vs 32.8%
p-value: p=0.62
The ACE gene insertion/deletion polymorphism is not associated with the risk of angiographic restenosis or adverse clinical events after coronary stent placement.
ACE I/D genotyping lacks utility for restenosis risk stratification post-stenting; leaves open any broader genetic role pending prospective trials.
Background —The renin-angiotensin system is thought to play a role in coronary thrombosis and restenosis. Plasma angiotensin I-converting enzyme (ACE) activity is associated with an insertion/deletion polymorphism in the gene coding for ACE. The objective of this study was to test the hypothesis that the D allele of the ACE gene is associated with a higher risk for restenosis after coronary stent placement. Methods and Results —This prospective study included 1850 consecutive patients with coronary artery disease who underwent intracoronary stent implantation. The adverse clinical events recorded were death, myocardial infarction, and target vessel revascularization. The primary end point of the study was restenosis (≥50% diameter stenosis at follow-up angiography performed in 84% of the patients). The secondary end point was clinical outcome 1 year after the procedure. The restenosis rate at the 6-month angiographic follow-up was 32.8% in patients with the II genotype, 34.0% for patients with the ID genotype, and 31.2% for patients with the DD genotype ( P =0.62). One-year event-free survival was 77.7% in patients with genotype II, 75.2% in patients with genotype ID, and 75.5% in patients with genotype DD ( P =0.54). The lack of association was also present in the subgroup of patients with a low risk for restenosis: the restenosis rate was 21.7% in II carriers, 23.4% in ID carriers, and 19.7% in DD carriers ( P =0.83). Conclusions —The ACE DD genotype or D allele does not influence the 1-year clinical and angiographic outcome of patients undergoing coronary stent placement. These data suggest that routine determination of the ACE genotype may not help identify patients who are at a higher risk of thrombotic and restenotic events after coronary stent placement.
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Koch et al. (2000) conducted a cohort in Coronary artery disease (n=1,850). ACE gene D allele / DD genotype vs. II and ID genotypes was evaluated on Restenosis (≥50% diameter stenosis at follow-up angiography) (p=0.62). The ACE DD genotype or D allele was not associated with a higher risk of restenosis at 6 months after coronary stent placement compared to II or ID genotypes (31.2% vs 32.8% and 34.0%; P=0.62).
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