Recurrent In-Stent Restenosis is Not Associated with the Angiotensin-Converting Enzyme D/I, Angiotensinogen Thr174Met and Met235

Examined genetic polymorphisms of the RAS.
Table 1
Table 2
Author(s): 

#aC. Michael Gross, MD, #aAndreas Perrot, MSc, aChristian Geier, MD, aMaximillian G. Posch, MD,
aSabine Hassfeld, MD, cJochen Krämer, MD, aSibylle Schmidt, MSc, aWolfgang Derer, MD,
aRainer Dietz, MD, a,b,*Cemil Özcelik, MD


Genotype analysis revealed that the incidence of RISR was not associated with any of the polymorphisms examined in this study. The distribution of ACE D/I genotypes was D/D 8 (20.5%), D/I 29 (74.4%), and I/I 2 (5.1%) in the ISR group versus D/D 11 (26.2%), D/I 27 (64.3%) and I/I 4 (9.5%) in the RISR group (chi-square 1.1, n.s., Table 2). Furthermore, there were no significant differences in allele findings in the AGT Thr174Met (C/C 79.5%, T/C 18%, T/T 2.5%, vs. 69%, 26.2%, 4.8%, chi-square 1.18, n.s.), and AGT Met235Thr (T/T 38.4%, T/C 46.2%, C/C 15.4% vs. 35.7%, 47.6%, 16.7%, chi-square 0.07, n.s.) genotype. The distribution of AGTR1 alleles was A/A 23 (59%), A/C 14 (35.9%) and C/C 2 (5.1%) in the ISR group, and A/A 19 (45.3%), A/C 20 (47.6%) and C/C 3 (7.1%) in the RISR group, respectively.



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