The relationship between ACE insertion/deletion polymorphism and coronary artery disease with or without myocardial infarction

dc.contributor.authorSeckin, D
dc.contributor.authorIlhan, N
dc.contributor.authorIlhan, N
dc.contributor.authorOzbay, Y
dc.date.accessioned2026-08-12T17:29:13Z
dc.date.issued2006
dc.departmentFırat Üniversitesi
dc.description.abstractObjectives: Presence of the D allele or homozygosity for the deletion (D) allele of the angiotensicen-converting enzyme (ACE) insertion/ deletion (I/D) polymorphism has been discussed as potent risk factor for coronary artery disease (CAD) and myocardial infarction (MI). The D allele is associated with higher levels of circulating ACE and therefore may predispose one to cardiovascular damage. Design and methods: The study presented here was performed to investigate the association between the ACE genotype and ACE levels. The study group was comprised of 118 angiographically verified CAD patients. 65 patients were MI (+) and 53 patients were MI (-) in this group. A total of 70 healthy individuals were taken as controls. Genomic DNA of 188 subjects was extracted from whole blood. The polymerase chain reaction was used for ACE genotyping, and ACE levels were measured by ELISA. Results: The D allele was found to be significantly more frequent in patients with MI (+) compared with controls (P = 0.024). ACE levels were significantly higher in both MI (-) and MI (+) groups with CAD patients than in controls (P < 0.005). Plasma ACE level was higher in all three groups in the DD genotype compared to II genotype. In groups I and III, this was statistically significant (P < 0.0001, P < 0.01). Conclusions: It was shown that the I/D polymorphism in the gene for ACE is a genetic risk factor for CAD patients who have a history of MI. ACE insertion/deletion gene polymorphism is also associated with plasma ACE levels in CAD patients with a history of MI. (c) 2005 The Canadian Society of Clinical Chemists. All rights reserved.
dc.identifier.doi10.1016/j.clinbiochem.2005.10.003
dc.identifier.endpage54
dc.identifier.issn0009-9120
dc.identifier.issn1873-2933
dc.identifier.issue1
dc.identifier.orcid0000-0001-9997-0418
dc.identifier.orcid0000-0002-0208-8929
dc.identifier.orcid0000-0001-9997-0418
dc.identifier.orcid0000-0002-0208-8929
dc.identifier.pmid16303122
dc.identifier.scopus2-s2.0-29344445008
dc.identifier.scopusqualityQ2
dc.identifier.startpage50
dc.identifier.urihttps://doi.org/10.1016/j.clinbiochem.2005.10.003
dc.identifier.urihttps://hdl.handle.net/11508/55621
dc.identifier.volume39
dc.identifier.wosWOS:000234793600007
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofClinical Biochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectcoronary artery disease
dc.subjectmyocardial infarction
dc.subjectACE I/D gene polymorphism
dc.titleThe relationship between ACE insertion/deletion polymorphism and coronary artery disease with or without myocardial infarction
dc.typeArticle

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