(Circulation. 2000;102:197.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Insertion/Deletion Polymorphism of the Angiotensin I-Converting Enzyme Gene Is Not Associated With Restenosis After Coronary Stent Placement
From Deutsches Herzzentrum München and 1. Medizinische Klinik rechts der Isar, Technische Universität München, Munich, Germany.
Correspondence to Dr Adnan Kastrati, Deutsches Herzzentrum, Lazarettstr 36, 80636 München, Germany. E-mail kastrati{at}dhm.mhn.de
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.
Key Words: genes • stents • angiotensin • restenosis • thrombosis
This article has been cited by other articles:
 |
|
 |
|
  W. Koch, W. Latz, M. Eichinger, C. Ganser, A. Schomig, and A. Kastrati Genotyping of the Angiotensin I-Converting Enzyme Gene Insertion/Deletion Polymorphism by the TaqMan Method Clin. Chem., August 1, 2005; 51(8): 1547 - 1549. [Full Text] [PDF]
|
|
|
|
 |
|
 L. J Wagenaar, A. J van Boven, A. C van der Wal, G. Amoroso, R. A Tio, C. M van der Loos, A. E Becker, and W. H van Gilst Differential localisation of the renin-angiotensin system in de-novo lesions and in-stent restenotic lesions in in-vivo human coronary arteries Cardiovasc Res, October 1, 2003; 59(4): 980 - 987. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Roguin, W. Koch, A. Kastrati, D. Aronson, A. Schomig, and A. P. Levy Haptoglobin Genotype Is Predictive of Major Adverse Cardiac Events in the 1-Year Period After Percutaneous Transluminal Coronary Angioplasty in Individuals With Diabetes Diabetes Care, September 1, 2003; 26(9): 2628 - 2631. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Koch, J. Mehilli, N. von Beckerath, C. Bottiger, A. Schomig, and A. Kastrati Angiotensin I-converting enzyme (ACE) inhibitors and restenosis after coronary artery stenting in patients with the DD genotype of the ACE gene J. Am. Coll. Cardiol., June 4, 2003; 41(11): 1957 - 1961. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Schieffer and H. Drexler The race for ACE: A simple answer to the controversial puzzle of angiotensin-converting enzyme (ACE) polymorphisms J. Am. Coll. Cardiol., June 4, 2003; 41(11): 1962 - 1963. [Full Text] [PDF]
|
|
|
|
 |
|
 M Hamon, S Fradin, A Denizet, E Filippi-Codaccioni, G Grollier, and R Morello Prospective evaluation of the effect of an angiotensin I converting enzyme gene polymorphism on the long term risk of major adverse cardiac events after percutaneous coronary intervention Heart, March 1, 2003; 89(3): 321 - 325. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A.H. Gomma, M.A. Elrayess, C.J. Knight, E. Hawe, K.M. Fox, and S.E. Humphries The endothelial nitric oxide synthase (Glu298Asp and -786T>C) gene polymorphisms are associated with coronary in-stent restenosis Eur. Heart J., December 2, 2002; 23(24): 1955 - 1962. [Abstract] [PDF]
|
|
|
|
 |
|
 F. Bonnici, B. Keavney, R. Collins, and J. Danesh Angiotensin converting enzyme insertion or deletion polymorphism and coronary restenosis: meta-analysis of 16 studies BMJ, September 7, 2002; 325(7363): 517 - 520. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Chan Review: Developments in restenosis Journal of Renin-Angiotensin-Aldosterone System, September 1, 2002; 3(3): 145 - 149. [Abstract] [PDF]
|
|
|
|
|
|
S. Humphries, C. Bauters, A. Meirhaeghe, L. Luong, M. Bertrand, and P. Amouyel The 5A6A polymorphism in the promoter of the stromelysin-1 (MMP3) gene as a risk factor for restenosis Eur. Heart J., May 1, 2002; 23(9): 721 - 725. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. R. P. Agema, J. W. Jukema, S. N. Pimstone, and J. J. P. Kastelein Genetic aspects of restenosis after percutaneous coronary interventions;towards more tailored therapy Eur. Heart J., November 2, 2001; 22(22): 2058 - 2074. [PDF]
|
|
|
|
|
|
E. Jorgensen, H. Kelbaek, S. Helqvist, G. V. H. Jensen, K. Saunamaki, J. Kastrup, O. Havndrup, H. Bundgaard, J. Kyst Madsen, M. Christiansen, et al. Predictors of coronary in-stent restenosis: importance of angiotensin-converting enzyme gene polymorphism and treatment with angiotensin-converting enzyme inhibitors J. Am. Coll. Cardiol., November 1, 2001; 38(5): 1434 - 1439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. P. Rossi, S. Taddei, A. Virdis, L. Ghiadoni, G. Albertin, S. Favilla, I. Sudano, A. C. Pessina, and A. Salvetti Exclusion of the ACE D/I Gene Polymorphism as a Determinant of Endothelial Dysfunction Hypertension, February 1, 2001; 37(2): 293 - 300. [Abstract] [Full Text] [PDF]
|
|