A potential role for the CDH13/CDH15 gene in repeat revascularization after first percutaneous coronary intervention
Abstract
Aim: Major drawbacks of percutaneous coronary intervention are the high occurrence of repeat revascularization due to restenosis and disease progression. The aim of this study was to find genetic indicators to predict the risk of repeat revascularization. Materials & methods: From April 2015 to June 2016, 143 patients with percutaneous coronary intervention with genetic test results were enrolled. SNPs were measured by OmniZhongHua-8, and the SNPs in pathways genes related to known stenosis-related processes from the KEGG, BioCarta and Gene Cards databases were selected for analysis. Results: Cell–extracellular matrix interactions were the pathways with the most significant SNP (CDH15 rs72819363) association with repeat revascularization. Compared with CDH13 rs11859453G carriers, the adjusted odds ratio for A carriers was 0.25 and 0.33 at 18 and 30 months. Conclusion: We demonstrated a potential role of the cell–extracellular matrix interactions pathway and the possible biomarker CDH13/CDH15 in the development of coronary repeat revascularization.
References
- 1. ST-segment elevation myocardial infarction in China from 2001 to 2011 (the China PEACE-Retrospective Acute Myocardial Infarction Study): a retrospective analysis of hospital data. Lancet 385, 441–451 (2015).
- 2. Prediction of long-term mortality after percutaneous coronary intervention in older adults results from the National Cardiovascular Data Registry. Circulation 125, 1501–1510 (2012).
- 3. 2017-Cardiovascular disease report in China – outline. Chin. Circ. J. 33(1), 1–8 (2018).
- 4. Drug eluting stents: an updated meta-analysis of randomized controlled trials. Heart 92, 641–649 (2006).
- 5. Authors/Task Force members, 2014 ESC/EACTS Guidelines on myocardial revascularization: the task force on myocardial revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur. Heart J. 35(37), 2541–2619 (2014).
- 6. Restenosis after PCI. Part 1: pathophysiology and risk factors. Nat. Rev. Cardiol. 9, 53–62 (2012).
- 7. . A genome wide association analysis in the GENDER study. Neth. Heart J. 17(6), 262–264 (2009).
- 8. . Association of ACE insertion or deletion polymorphisms with the risk of coronary restenosis after percutaneous coronary intervention: a meta-analysis. J. Renin Angiotensin Aldosterone Syst. 16(4), 844–850 (2015).
- 9. Relationship of paraoxonase-1 Q192R genotypes and in-stent restenosis and re-stenting in Chinese patients after coronary stenting. Atherosclerosis 251, 305–310 (2016).
- 10. Matrix metalloproteinases 2 and 3 gene polymorphisms and the risk of target vessel revascularization after percutaneous coronary intervention: is there still room for determining genetic variation of MMPs for assessment of an increased risk of restenosis? Dis. Markers 29(5), 265–273 (2010).
- 11. Platelet response to clopidogrel and restenosis in patients treated predominantly with drug-eluting stents. Am. Heart J. 160(2), 355–361 (2010).
- 12. Fast and accurate genotype imputation in genome-wide association studies through pre-phasing. Nat. Genet. 44(8), 955–959 (2012).
- 13. 1000 Genomes Project Consortium, A global reference for human genetic variation. Nature 526(7571), 68–74 (2015).
- 14. GTEx. www.gtexportal.org/home/gene/
- 15. Pathway analysis using genome-wide association study data for coronary restenosis – a potential role for the PARVB gene. PLoS ONE 8(8), e70676 (2013).
- 16. Alterations in CDH15 and KIRREL3 in patients with mild to severe intellectual disability. Am. J. Hum. Genet. 83(6), 703–713 (2008).
- 17. Regulation of contractile signaling and matrix remodeling by T-cadherin in vascular smooth muscle cells: constitutive and insulin-dependent effects. Cell. Signal. 26(9), 1897–908 (2014).
- 18. Adiponectin receptors, with special focus on the role of the third receptor, T-cadherin, in vascular disease. Med. Mol. Morphol. 40(3), 115–120 (2007).
- 19. Genome-wide scan identifies CDH13 as a novel susceptibility locus contributing to blood pressure determination in two European populations. Hum. Mol. Genet. 18(12), 2288–2296 (2009).
- 20. A genome-wide association study reveals a quantitative trait locus of adiponectin on CDH13 that predicts cardiometabolic outcomes. Diabetes 60(9), 2417–2423 (2011).
- 21. Genetic variation in CDH13 is associated with lower plasma adiponectin levels but greater adiponectin sensitivity in east Asian populations. Diabetes 62(12), 4277–4283 (2013).
- 22. Effect of the stromelysin-1 promoter on efficacy of pravastatin in coronary atherosclerosis and restenosis. Am. J. Cardiol. 83(6), 852–856 (1999).
- 23. The 5A6A polymorphism in the promoter of the stromelysin-1 (MMP3) gene as a risk factor for restenosis. Eur. Heart J. 23(9), 721–725 (2002).
- 24. The 5A/6Apolymorphismofthestromelysin-1geneandrestenosis after percutaneous coronary interventions. Eur. Heart J. 25, 335–341 (2004).
- 25. Matrix metalloproteinases 2 and 3 gene polymorphisms and the risk of target vessel revascularization after percutaneous coronary intervention: is there still room for determining genetic variation of MMPs for assessment of an increased risk of restenosis? Dis. Markers 29(5), 265–273 (2010).
- 26. Duration of dual antiplatelet therapy after drug-eluting stent implantation: a systematic review and meta-analysis of randomized controlled trials. J. Am. Coll. Cardiol. 65(13), 1298–1310 (2015).