PMID- 32093874 OWN - NLM STAT- MEDLINE DCOM- 20201015 LR - 20201015 IS - 1879-114X (Electronic) IS - 0149-2918 (Linking) VI - 42 IP - 3 DP - 2020 Mar TI - Associations Between Polymorphisms of Endothelial Nitric Oxide Synthase, Matrix Metalloproteinase 3, Angiotensinogen, and Angiotensin II Type 1 Receptor and Risk of Restenosis After Percutaneous Coronary Intervention: A Meta-analysis. PG - 458-474 LID - S0149-2918(20)30054-0 [pii] LID - 10.1016/j.clinthera.2020.01.018 [doi] AB - PURPOSE: Previous studies have reported controversial results regarding the risk of restenosis with polymorphisms of endothelial nitric oxide synthase (eNOS), matrix metalloproteinase 3 (MMP-3), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT1R) after percutaneous coronary intervention (PCI). This study aimed to summarize the association between these polymorphisms and risk of restenosis after PCI. METHODS: We searched the electronic databases of PubMed, Embase, Cochrane's Library, and ClinicalTrials.gov for studies on the association of eNOS, MMP-3, AGT, and AT1R polymorphisms with restenosis. FINDINGS: A total of 17 studies (7781 patients) were analyzed, including 5 studies on eNOS G298A (n = 912), 5 studies on MMP3 5A/6A (n = 4519), 6 studies on AGT M235T (n = 1801), and 7 studies on AT1R A1166C (n = 2477). For the G298A variant of the eNOS gene, the allele odds ratio (OR) was 1.685 (95% CI, 1.269-2.338; P < 0.001), the heterozygote OR was 2.144 (95% CI, 1.490-3.085; P < 0.001), the dominant OR was 2.078 (95% CI, 1.462-2.954; P < 0.001), and the overdominant OR was 0.496 (95% CI, 0.348-0.706; P < 0.001). For the 5A/6A variant of the MMP3 gene, the heterozygote OR was 0.839 (95% CI, 0.722-0.975; P = 0.022), the dominant OR was 0.846 (95% CI, 0.733-0.976; P = 0.022), and the overdominant OR was 1.141 (95% CI, 1.001-1.301; P = 0.049). For the M235T variant of the AGT gene, the heterozygote OR was 1.594 (95% CI, 1.179-2.155; P = 0.002), the dominant OR was 1.437 (95% CI, 1.077-1.918; P = 0.014), and the overdominant OR was 0.694 (95% CI, 0.555-0.869; P = 0.001). Positive results were observed in the AT1R gene A1166C polymorphism under 3 models (homozygote OR = 2.009; 95% CI, 1.433-2.816; P < 0.001; recessive OR 1.874; 95% CI, 1.353-2.595; P < 0.001; and dominant OR = 1.350; 95% CI, 1.105-1.649; P = 0.003). IMPLICATIONS: The G298A variant of eNOS, the 5A/6A variant of MMP3, the M235T variant of AGT, and the A1166C variant of A1TR may increase the risk of restenosis after PCI. CI - Copyright (c) 2020 The Authors. Published by Elsevier Inc. All rights reserved. FAU - Zhou, Shuang AU - Zhou S AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China; Department of Pharmacy Administration and Clinical Pharmacy, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China. FAU - Mu, Guangyan AU - Mu G AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China; Department of Pharmacy Administration and Clinical Pharmacy, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China. FAU - Wei, Shaopeng AU - Wei S AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China. FAU - Liu, Zhiyan AU - Liu Z AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China; Department of Pharmacy Administration and Clinical Pharmacy, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China. FAU - Wang, Zhe AU - Wang Z AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China. FAU - Xiang, Qian AU - Xiang Q AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China. FAU - Cui, Yimin AU - Cui Y AD - Department of Pharmacy, Peking University First Hospital, Beijing, People's Republic of China; Department of Pharmacy Administration and Clinical Pharmacy, School of Pharmaceutical Sciences, Peking University, Beijing, People's Republic of China. Electronic address: cui.pharm@pkufh.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20200221 PL - United States TA - Clin Ther JT - Clinical therapeutics JID - 7706726 RN - 0 (AGT protein, human) RN - 0 (Receptor, Angiotensin, Type 1) RN - 11002-13-4 (Angiotensinogen) RN - EC 1.14.13.39 (NOS3 protein, human) RN - EC 1.14.13.39 (Nitric Oxide Synthase Type III) RN - EC 3.4.24.17 (MMP3 protein, human) RN - EC 3.4.24.17 (Matrix Metalloproteinase 3) SB - IM MH - Angiotensinogen/*genetics MH - Coronary Stenosis/epidemiology/genetics/surgery MH - Genetic Predisposition to Disease MH - Humans MH - Matrix Metalloproteinase 3/*genetics MH - Nitric Oxide Synthase Type III/*genetics MH - *Percutaneous Coronary Intervention/adverse effects/statistics & numerical data MH - Polymorphism, Single Nucleotide/genetics MH - Postoperative Complications/epidemiology/genetics/surgery MH - Receptor, Angiotensin, Type 1/*genetics MH - Recurrence OTO - NOTNLM OT - AGT OT - AT1R OT - MMP-3 OT - eNOS OT - polymorphisms OT - risk of restenosis COIS- Disclosures The authors have indicated that they have no conflicts of interest regarding the content of this article. EDAT- 2020/02/26 06:00 MHDA- 2020/10/21 06:00 CRDT- 2020/02/26 06:00 PHST- 2019/11/07 00:00 [received] PHST- 2020/01/22 00:00 [revised] PHST- 2020/01/26 00:00 [accepted] PHST- 2020/02/26 06:00 [pubmed] PHST- 2020/10/21 06:00 [medline] PHST- 2020/02/26 06:00 [entrez] AID - S0149-2918(20)30054-0 [pii] AID - 10.1016/j.clinthera.2020.01.018 [doi] PST - ppublish SO - Clin Ther. 2020 Mar;42(3):458-474. doi: 10.1016/j.clinthera.2020.01.018. Epub 2020 Feb 21.