Association of ACE insertion or deletion polymorphisms with the risk of coronary restenosis after percutaneous coronary intervention: A meta-analysis

Abstract

Objective: Previous case-control studies on the relationship between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphisms and coronary restenosis did not reach the same conclusion. In the present study, we aimed to further evaluate the relationship between the ACE gene I/D polymorphisms and coronary restenosis, after percutaneous coronary intervention (PCI). Methods: By searching PubMed, EMBase, the Chinese Biomedical Literature Database and Wanfang database, we selected 16 case-control studies related to ACE gene I/D polymorphism and coronary restenosis after PCI. To test for heterogeneity in each study, we utilized the Q-test and I2 test. To merge the odds ratio (OR) and 95% CI, we utilized the random effects model during the analyses. Results: The present study included 4693 subjects: 1241 patients with coronary restenosis and 3452 without coronary restenosis. By meta-analysis, we found there was significant association of ACE gene I/D polymorphism with coronary restenosis (D allele versus I allele: OR = 1.92; 95% CI (1.40–2.43); p < 0.001). A subgroup analysis, by stratification according to ethnicity, also showed that this association was found not only in the Caucasian population ((D allele versus I allele: OR = 1.94; 95% CI (1.38–2.80); p < 0.001)), but also in the Asian population ((D allele versus I allele: OR = 1.83; 95% CI (1.05–3.20); p = 0.03)). After stratification according to age, we found that the D allele carriers have a higher risk for development of coronary restenosis in subjects < 60 years old (OR = 2.13; 95% CI: 1.40–3.24; p = 0.0004); while in the subjects ⩾ 60 years old, the association was present with bordering significance (OR = 1.48; 95%CI: 0.98–2.25; p = 0.06). Conclusions: The present study suggested that the ACE gene I/D polymorphism was associated with coronary restenosis, regardless of age and ethnicity.

Angiotensin-Converting Enzyme Gene Deletion Polymorphism is Associated with Lymph Node Metastasis in Colorectal Cancer Patients in a Chinese Population

“…This individual susceptibility may be determined by small changes in genes. Previous studies reported that ACE gene I/D polymorphism was associated with different cancer risk [ 33 , 34 ]. I/D polymorphism is an insertion or deletion polymorphism with −287bp in ACE gene.…”

Association of angiotensin‐converting enzyme insertion/deletion polymorphism with susceptibility to systemic lupus erythematosus: a meta‐analysis

“…Miao et al . conducted a meta‐analysis to investigate the association between ACE I/D gene polymorphism and risk of coronary restenosis after percutaneous coronary intervention, and found that D allele was associated with coronary restenosis . Yuan et al .…”

“…Miao et al conducted a meta-analysis to investigate the association between ACE I/D gene polymorphism and risk of coronary restenosis after percutaneous coronary intervention, and found that D allele was associated with coronary restenosis. 41 Yuan et al performed a meta-analysis to explore the relationship between ACE I/D gene polymorphism and risk of ischemic stroke, and found that the genotype DD of ACE could increase the risk of ischemic stroke. 42 Zintzaras et al performed a meta-analysis to discuss the correlation between ACE I/D gene polymorphism and coronary artery disease, and found that the D allele and DD genotype were related to the onset of coronary artery disease.…”

Alterations in ACE and ABCG2 expression levels in the testes of rats subjected to atropine-induced toxicity

“…ACE is involved in the physiology of the vasculature, blood pressure and inflammation (24). It has been demonstrated that the insertion/deletion (I/D) ACE gene polymorphism is associated with coronary restenosis (25), and may also affect blood Positive ISH staining appears as brown staining. Total ACE integrated optical density in the testes of rats subjected to atropine exposure was significantly reduced compared with control rats (Table II; (27).…”