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ACE ABSTRACTS: D Allele of the Angiotensin I-Converting Enzyme Is a Major Risk Factor for Restenosis After Coronary Stenting.

Carole Amant, BS; Christophe Bauters, MD; Jean-Christophe Bodart, MD; Jean-Marc Lablanche, MD; Gilles Grollier, MD; Nicolas Danchin, MD; Martial Hamon, MD; Florence Richard, MD; Nicole Helbecque, PhD; Eugène P. McFadden, MRCPI; Philippe Amouyel, MD, PhD; ; Michel E. Bertrand, MD Hôpital Cardiologique, Lille Cedex, France. [Circulation. 1997;96:56-60]

BACKGROUND: Although intracoronary stent implantation significantly reduces restenosis compared with balloon angioplasty, a minority of patients still develop restenosis predominantly due to neointimal hyperplasia. Experimental studies suggest that the renin-angiotensin system is involved in neointimal hyperplasia after arterial injury. In humans, the plasma and cellular levels of ACE are associated with an I/D genetic polymorphism in the ACE gene, DD patients having higher levels.

METHODS AND RESULTS: We investigated a possible relation between the ACE I/D polymorphism and restenosis in 146 patients who underwent successful implantation of a Palmaz-Schatz stent and had 6-month follow-up angiography. The minimal lumen diameter (MLD) before and after the procedure did not differ significantly among the three groups of genotypes (DD, ID, and II). At follow-up, MLD had a significant inverse relationship to the number of D alleles present (DD, 1.65±0.71 mm; ID, 1.84±0.60 mm; II, 2.05±0.61 mm; P<.007). Late luminal loss during the follow-up period was significantly related to the number of D alleles (DD, 0.89±0.61 mm; ID, 0.60±0.52 mm; II, 0.40±0.53 mm; P<.0001). The relative risk of restenosis (defined as a >50% diameter stenosis at follow-up) approximated by the adjusted odds ratio was 2.00 per number of D alleles (95% confidence interval, 1.03 to 3.88, P<.04).

CONCLUSIONS: The ACE I/D polymorphism influences the level of late luminal loss after coronary stent implantation. These results suggest that the renin-angiotensin system may be implicated in the pathogenesis of restenosis after coronary stenting.

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