Correlation of angiotensin I-converting enzyme gene insertion/deletion polymorphism with rheumatic heart disease: a

Yulong Tian1, Zhongchun Ge1, Yuliang Xing1

  • 1Department of Cardiology, People's Hospital of Xuyi, Xuyi 211700, Jiangsu, P.R. China.

Bioscience Reports
|October 21, 2016
PubMed

Insights

This study found no significant link between the ACE I/D gene variant and rheumatic heart disease (RHD) risk. Further research with larger sample sizes is needed to confirm these findings on RHD susceptibility.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Epidemiology
  • Rheumatic Heart Disease Research

Background:

  • Rheumatic heart disease (RHD) poses a significant global cardiovascular health burden.
  • Previous studies suggest a potential link between the angiotensin I-converting enzyme gene insertion/deletion (ACE I/D) polymorphism and RHD susceptibility, but findings are inconsistent.

Purpose of the Study:

  • To conduct a meta-analysis to precisely estimate the association between the ACE I/D variant and RHD risk.
  • To investigate potential influences of ethnicity and RHD severity on this relationship.

Main Methods:

  • Systematic literature search for case-control studies published between January 2000 and 2016.
  • Meta-analysis of nine selected studies, comprising 1333 RHD patients and 1212 healthy controls.
  • Calculation of odds ratios (OR) with 95% confidence intervals (CI) to assess the strength of association.

Main Results:

  • No statistically significant association was detected between ACE I/D polymorphism and RHD risk across all genetic models (P > 0.05).
  • Subgroup analysis by ethnicity, including Asian populations, also revealed no significant relationship.
  • No significant differences in ACE I/D polymorphism frequency were observed concerning RHD severity (mitral valve lesion, combined valve lesion) or sex.

Conclusions:

  • The ACE I/D polymorphism does not appear to be a significant risk factor for rheumatic heart disease progression based on current evidence.
  • The findings highlight the need for larger, well-designed studies to definitively confirm or refute the role of ACE I/D polymorphism in RHD.

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