INTERVENTIONAL CARDIOLOGY
Predictors of coronary in-stent restenosis: importance of angiotensin-converting enzyme gene polymorphism and treatment with angiotensin-converting enzyme inhibitors
Erik Jørgensen, MD*,*,
Henning Kelbæk, MD*,
Steffen Helqvist, MD*,
Gunnar V. H. Jensen, MD*,
Kari Saunamäki, MD*,
Jens Kastrup, MD*,
Ole Havndrup, MD*,
Henning Bundgaard, MD*,
Jan Kyst Madsen, MD*,
Michael Christiansen, MD ,
Paal S. Andersen, PhD and
Johan H. C. Reiber, PhD
* Department of Cardiology, The Heart Centre, Rigshospitalet, Copenhagen, Denmark
the Department of Clinical Biochemistry, Statens Serum Institute, Copenhagen, Denmark
Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands
Manuscript received March 12, 2001;
revised manuscript received June 14, 2001,
accepted July 12, 2001.
* Reprint requests and correspondence: Dr. Erik Jørgensen, 2014 Cardiac Catheterisation Laboratory, Department of Cardiology, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark
erikj{at}rh.dk
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.
|
Abbreviations and Acronyms
| | ACE | = angiotensin-converting enzyme | | DANSTENT | = Danish Randomized Multicenter Trial of Coronary Restenosis After Treatment with the NIR and the Palmaz-Schatz Stent | | DD | = homozygotes with two deletion alleles in the ACE gene | | D/I | = deletion/insertion | | DI | = heterozygotes with one deletion and one insertion allele in the ACE gene | | II | = homozygotes with two insertion alleles in the ACE gene | | PTCA | = percutaneous transluminal coronary angioplasty | | QCA | = quantitative coronary angiography |
|
This article has been cited by other articles:
|
|
|
|
 
R. S. Ripa, E. Jorgensen, Y. Wang, J. J. Thune, J. C. Nilsson, L. Sondergaard, H. E. Johnsen, L. Kober, P. Grande, and J. Kastrup
Stem Cell Mobilization Induced by Subcutaneous Granulocyte-Colony Stimulating Factor to Improve Cardiac Regeneration After Acute ST-Elevation Myocardial Infarction: Result of the Double-Blind, Randomized, Placebo-Controlled Stem Cells in Myocardial Infarction (STEMMI) Trial
Circulation,
April 25, 2006;
113(16):
1983 - 1992.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Kelbaek, L. Thuesen, S. Helqvist, L. Klovgaard, E. Jorgensen, S. Aljabbari, K. Saunamaki, L. R. Krusell, G. V.H. Jensen, H. E. Botker, et al.
The Stenting Coronary Arteries in Non-stress/benestent Disease (SCANDSTENT) Trial
J. Am. Coll. Cardiol.,
January 17, 2006;
47(2):
449 - 455.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Kelbaek, L. Thuesen, S. Helqvist, L. Klovgaard, E. Jorgensen, S. Aljabbari, K. Saunamaki, L. R. Krusell, G. V.H. Jensen, H. E. Botker, et al.
The Stenting Coronary Arteries in Non-stress/benestent Disease (SCANDSTENT) Trial
J. Am. Coll. Cardiol.,
December 13, 2005;
(2005)
j.jacc.2005.10.045v1.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
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]
|
|
|
|
|
|
|
S. C. Wolf, G. Sauter, H.-P. Rodemann, T. Risler, and B. R. Brehm
Influence of growth factors on the proliferation of vascular smooth muscle cells isolated from subtotally nephrectomized rats after endothelin or angiotensin II antagonism
Nephrol. Dial. Transplant.,
February 1, 2005;
20(2):
312 - 318.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Lerman
Restenosis: Another "Dysfunction" of the Endothelium
Circulation,
January 4, 2005;
111(1):
8 - 10.
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. A. Artz, L. B. Hilbrands, G. Borm, K. J. M. Assmann, and J. F. M. Wetzels
Blockade of the renin-angiotensin system increases graft survival in patients with chronic allograft nephropathy
Nephrol. Dial. Transplant.,
November 1, 2004;
19(11):
2852 - 2857.
[Abstract]
[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]
|
|
|
|
|
|
|
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]
|
|
|
|
|
|
|
D. S. Jacoby and D. J. Rader
Renin-Angiotensin System and Atherothrombotic Disease: From Genes to Treatment
Arch Intern Med,
May 26, 2003;
163(10):
1155 - 1164.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Ribichini, V. Ferrero, W. Wijns, G. Matullo, A. Piazza, E. Uslenghi, J. L. Zhuo, F. A.O. Mendelsohn, and M. Ohishi
Can ACE Inhibitors Promote Detrimental Vascular Effects After Percutaneous Injury? * Response
Hypertension,
October 1, 2002;
e6(4):
.
[Full Text]
[PDF]
|
|
|
|
