Abstract

BackgroundCSR-CSA is frequent in patients with CHF. Dilated cardiomyopathy (DCM) is a structural heart disease with strong genetic background, yet one of the leading etiological causes of CHF. Studies have showed that the HSPB7 gene is associated with DCM. ObjectivesWe aimed to explore the prevalence of polymorphisms of the HSPB7 gene in the Chinese Han population with CSR-CSA and CHF caused by DCM. MethodsA total of 503 unrelated subjects of the Chinese Han population, including 283 CHF patients caused by DCM and 220 healthy controls, were involved in the study. The CHF patients were classified as the CSA-CHF group and the non-CSA-CHF group according to the PSG parameters. The rs1739843 polymorphisms of the HSPB7 gene were identified by real-time quantitative polymerase chain reaction. ResultsIn the present study, 35.8% of CHF patients caused by DCM had CSR-CSA. Comparison demonstrated that the CSA-CHF group had significantly higher TT genotype and T allele frequencies in the rs1739843 single nucleotide polymorphism (SNP) of the HSPB7 gene. There were no significant differences among the CC genotype distribution of the CSA-CHF group and the non-CSA-CHF group or the control group. ConclusionsThe rs1739843 polymorphism of the HSPB7 gene might be involved in the pathogenesis of CSR-CSA and CHF subjects caused by DCM in the Chinese Han population. This finding was from a genetic search for the role of the HSPB7 gene in CSR-CSA of CHF patients caused by DCM.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.