Effect of AGTR1 A1166C genetic polymorphism on coronary artery lesions and mortality in patients with acute myocardial infarction

Abstract

The pathogenesis and prognosis of patients with acute myocardial infarction (AMI) may be influenced by both genetic and environmental factors. Findings on the relationship of polymorphisms in various genes encoding the renin-angiotensin-aldosterone system with coronary artery lesions and mortality in AMI patients are inconsistent. The aim of this study was to determine whether the AGTR1 A1166C genetic polymorphism affects coronary artery lesions and 1-year mortality in post-AMI patients. Patients with their first AMI admitted to Cho Ray Hospital, Vietnam, from January 2020 to August 2021 were enrolled in this prospective clinical study. All participants underwent invasive coronary angiography and were identified as having the genotypes of AGTR1 A1166C by way of a polymerase chain reaction method. All patients were followed up for all-cause mortality 12 months after AMI. The association of the AGTR1 A1166C polymorphism with coronary artery lesions and 1-year mortality was evaluated using logistic regression and Cox regression analysis, respectively. Five hundred and thirty-one AMI patients were recruited. The mean age was 63.9 ± 11.6 years, and 71.6% of the patients were male. There were no significant differences in the location and number of diseased coronary artery branches between the AA and AC+CC genotypes. The AC and CC genotypes were independently associated with ≥ 90% diameter stenosis of the left anterior descending (LAD) artery (odds ratio = 1.940; 95% confidence interval (CI): 1.059–3.552, p = 0.032). The 1-year all-cause mortality rate difference between patients with the AC and CC genotypes versus those with the AA genotype was not statistically significant (hazard ratio = 1.000, 95% CI: 0.429–2.328, p = 1.000). The AGTR1 A1166C genetic polymorphism is associated with very severe luminal stenosis of the LAD but not with mortality in AMI patients.

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

“…Altered expression of FA2H [441], DSCAM (DS cell adhesion molecule) [442], OLIG2 [328], PCDH15 [443], GRID2 [424], CTTNBP2 [444], AFF2 [445], SYNE2 [446] and EGFR (epidermal growth factor receptor) [447] are associated with autism spectrum disorder. FA2H [111], SERPINA1 [448], HOXB9 [113], TGM2 [449], LRRK2 [450], ROS1 [451], CFC1 [452], GDF3 [453], TF (transferrin) [121], RXFP1 [454], RELN (reelin) [455], HTR2C [456], MYL7 [457], DYSF (dysferlin) [458], GJA5 [459], IRX1 [460], TLL1 [461], SUCNR1 [462], KERA (keratocan) [463], TFAP2B [464], HOXA5 [465], ACSL6 [466], DSCAM (DS cell adhesion molecule) [467], MSR1 [468], REN (renin) [64], VEGFC (vascular endothelial growth factor C) [469], TLR2 [470], PCSK2 [471], FGF12 [472], SLC22A3 [142], HSPB7 [473], CSRP3 [474], KLRD1 [475], PTPRO (protein tyrosine phosphatase receptor type O) [476], IL7R [477], CUX2 [478], ACAN (aggrecan) [479], SHH (sonic hedgehog signaling molecule) [480], MEOX1 [481], AGTR1 [482], VTN (vitronectin) [483], SIRT2 [79], RBP4 [484], IL2RG [485], EPAS1 [486], CDH13 [487], TRPC6 [488], MMP3 [261], PCDHGA3 [489], FGF19 [490], TBX18 [491], HLA-DRB1 [492]. CD74 [493], VWF (von Willebrand factor) [267], MTTP (microsomal triglyceride transfer protein) [494], ANGPT2 [184], AKR1C3 [495], NEDD4L [496], CASP1 [497], LDB2 [498], CHRNA5 [499], CCND2 [500], BRCA2 [97], ZBTB20 […”