Polymorphic Variants of AGT, ABCA1, and CYBA Genes Influence the Survival of Patients with Coronary Artery Disease: A Prospective Cohort Study

Genes (Basel). 2022 Nov 18;13(11):2148. doi: 10.3390/genes13112148.

Abstract

Genetic factors can influence the risk of coronary artery disease (CAD) and the survival of patients. Our previous research led to the identification of genetic variants predisposing to CAD in the Polish population. Since many of them affect the clinical phenotype of the disease, the aim of this study was searching for genetic factors potentially influencing survival in patients with CAD. The study included 276 patients hospitalized due to coronary artery disease. The database of medical history and genotypic results of 29 polymorphisms were used. The endpoint was defined as death from cardiovascular causes. Survival was defined as the period from angiographic confirmation of CAD to death from cardiovascular causes. Three of all the analyzed genes were associated with survival. In the case of the AGT (rs699) and ABCA1 (rs2230806) genes polymorphisms, the risk of death was higher in GG homozygotes compared to the A allele carriers in the 10-year period. In the case of the CYBA (rs72811418) gene polymorphism, the effect on mortality was shown in both 5- and 10-year periods. The TA heterozygotes were predisposed to a higher risk of death than the TT homozygotes. Concluding, the AGT, ABCA1, and CYBA genes polymorphisms influence the risk of death in patients with CAD.

Keywords: coronary artery disease; polymorphism; survival.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter 1* / genetics
  • Alleles
  • Angiotensinogen* / genetics
  • Coronary Artery Disease* / genetics
  • Disease Susceptibility
  • Genotype
  • Humans
  • NADPH Oxidases* / genetics
  • NADPH Oxidases* / metabolism
  • Polymorphism, Genetic
  • Prospective Studies

Substances

  • ABCA1 protein, human
  • ATP Binding Cassette Transporter 1
  • CYBA protein, human
  • NADPH Oxidases
  • AGT protein, human
  • Angiotensinogen

Grants and funding

This research was supported by a grant PCN-1-072/N/0/Z from the Medical University of Silesia in Katowice.