Key result
ACE inhibitors are not linked to lower in-stent restenosis in DD genotype patients undergoing stenting.
Why the study?
Small studies suggested an unfavorable effect of ACE inhibitors on restenosis after coronary stenting in DD genotype carriers, questioning their use in these patients.
Do ACE inhibitors increase the risk of in-stent restenosis in patients with symptomatic coronary artery disease and the DD genotype of the ACE gene after stent implantation?
Cohort (n=612)
Do ACE inhibitors increase the risk of in-stent restenosis in patients with symptomatic coronary artery disease and the DD genotype of the ACE gene after stent implantation?
In patients with the ACE gene DD genotype undergoing coronary stenting, treatment with ACE inhibitors does not increase the risk of in-stent restenosis, contradicting previous smaller reports.
Supports safety of ACE inhibitors in DD patients post-stenting; leaves open need for randomized confirmation.
OBJECTIVES: We tested the hypothesis that patients with the DD genotype of the angiotensin I-converting enzyme (ACE) gene who are treated with ACE inhibitors are at a higher risk of restenosis after coronary stent placement than patients who do not receive ACE inhibitors. BACKGROUND: Two recent studies with a limited series of patients carrying the DD genotype suggested an unfavorable impact of the use of ACE inhibitors on the restenotic process after implantation of stents in coronary arteries. Because these findings may question the use of ACE inhibitors after coronary stenting, we examined this important issue in a large series of patients. METHODS: We determined the ACE gene I/D genotype of 2,222 consecutive patients with symptomatic coronary artery disease who underwent stent implantation. The patients with the DD genotype (n = 612) constituted the study population. The primary end point was in-stent restenosis, which was assessed as angiographic restenosis (> or =50% diameter stenosis at six-month follow-up) and clinical restenosis (need for target vessel revascularization due to symptoms or signs of ischemia in the presence of angiographic restenosis over one year after the intervention). RESULTS: Of the 612 patients with the DD genotype, 403 (65.8%) were treated with ACE inhibitors and 209 (34.2%) did not receive ACE inhibitors. The angiographic and clinical restenosis rates were not significantly different between the group treated with ACE inhibitors and the group not receiving ACE inhibitors (p = 0.55). Continuous measures of restenosis, minimal lumen diameter, diameter stenosis, late lumen loss, and loss index were also similar in both groups (p > or = 0.55). In addition, one-year survival free of myocardial infarction was not significantly different between the two groups (p = 0.27). CONCLUSIONS: In contrast to previous reports, our study provides evidence that patients carrying the DD genotype are not exposed to an increased risk of restenosis after stent placement when treated with ACE inhibitors.
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Koch et al. (2003) conducted a cohort in symptomatic coronary artery disease (n=612). ACE inhibitors vs. No ACE inhibitors was evaluated on in-stent restenosis (angiographic restenosis at 6 months and clinical restenosis over 1 year) (p=0.55). ACE inhibitor treatment in patients with the DD genotype undergoing coronary stenting did not significantly alter angiographic or clinical restenosis rates compared to no ACE inhibitors (p=0.55).
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