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Völzke H, Hertwig S, Rettig R. The Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene and the Risk for Restenosis After PTCA. Int J Angiol. 2000;9(2):82-86doi: 10.1007/BF01617046.
Völzke, H., Hertwig, S., & Rettig, R. (2000). The Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene and the Risk for Restenosis After PTCA. The International journal of angiology : official publication of the International College of Angiology, Inc, 9(2), 82-86. https://doi.org/10.1007/BF01617046
Völzke, et al. "The Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene and the Risk for Restenosis After PTCA." The International journal of angiology : official publication of the International College of Angiology, Inc vol. 9,2 (2000): 82-86. doi: https://doi.org/10.1007/BF01617046
Völzke H, Hertwig S, Rettig R. The Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene and the Risk for Restenosis After PTCA. Int J Angiol. 2000 Mar;9(2):82-86. doi: 10.1007/BF01617046. PMID: 10758202.
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Int J Angiol. 2000 Mar;9(2):82-86. doi: 10.1007/BF01617046.

The Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene and the Risk for Restenosis After PTCA.

The International journal of angiology : official publication of the International College of Angiology, Inc

Völzke, Hertwig, Rettig

Affiliations

  1. Clinic of Internal Medicine B, Ernst Moritz Arndt University, Greifswald, Germany

PMID: 10758202 DOI: 10.1007/BF01617046

Abstract

The therapeutic benefit of percutaneous transluminal coronary angioplasty (PTCA) is limited by restenosis in about 30% of patients. The underlying mechanisms are currently not well understood. Besides clinical and angiographic variables, genetic factors may be involved. We determined the angiotensin I-converting enzyme (ACE) I/D genotype as a possible risk factor for restenosis in 511 consecutive patients who had undergone successful PTCA and follow-up angiography. Clinical and angiographic variables were also considered as possible predictors of restenosis. One hundred sixty patients had restenosis as defined by a greater than 50% progression of residual stenosis of the dilated segment at follow-up angiography. There were significantly more patients with the ACE DD genotype in the restenosis than in the no-restenosis group. This difference did not remain statistically significant in an analysis of covariance that included genetic and clinical variables. Patients who subsequently developed restenosis had a higher degree of stenosis and more severe lesions before PTCA as well as less residual stenosis immediately after PTCA. We conclude that the ACE DD genotype is not an independent risk factor for restenosis after PTCA.

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