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Aim:We aimed to identify genetic variants associated with ACE inhibitor (ACEI)-induced cough.Materials & methods:A nested case–control study was performed among hypertensive Chinese patients receiving enalapril-only therapy. Whole-exome sequencing and genome-wide association analysis were performed. Results:We identified that PNPT1rs13015243 (odds ratio [OR]: 0.47; 95% CI: 0.34–0.66; p=7.45×10-6), PNPT1rs13009649 (OR: 0.48; 95% CI: 0.35–0.67; p=9.96×10-6) and PCGF3rs1044147 (OR: 2.67; 95% CI: 1.71–4.17; p=9.91×10-6) were significantly associated with ACEI-induced cough. Nearly genome-wide significant associations in previously reported candidate risk genes CLASP1, ACE, CES1, CPN1, XPNPEP1, PDE11Aor SLC38Awere detected in our dataset.Conclusion:Our results suggest that ACEI-induced cough is associated with noncoding SNPs of PNPT1and PCGF3, all of which are independent of the bradykinin pathway.Study registration:NCT03259399.

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 (CDH15rs72819363) association with repeat revascularization. Compared with CDH13rs11859453G 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/CDH15in the development of coronary repeat revascularization.