Factor XIII Val34Leu polymorphism in patients with cardiac syndrome X

Gamze Babur Güler1, Ulaankhuu Batgerel, Ekrem Güler

  • 1Istinye State Hospital, Istanbul, Turkey. gamzebabur@hotmail.com.

Cardiology Journal
|May 17, 2013
PubMed

Insights

The factor XIII Val34Leu polymorphism is more common in patients with cardiac syndrome X (CSX), suggesting a potential genetic link. This finding may aid in understanding CSX risk factors.

Area of Science:

  • Cardiology
  • Genetics
  • Molecular Biology

Background:

  • Cardiac Syndrome X (CSX) is characterized by chest pain despite normal coronary arteries.
  • Understanding the genetic underpinnings of CSX is crucial for risk stratification and management.
  • Factor XIII (FXIII) is involved in hemostasis and may play a role in thrombotic disorders.

Purpose of the Study:

  • To investigate the frequency of factor XIII gene polymorphism in patients diagnosed with cardiac syndrome X.
  • To determine if specific factor XIII variants are associated with an increased risk of developing CSX.

Main Methods:

  • A cross-sectional, observational study involving 48 female CSX patients and 36 age- and gender-matched controls.
  • CSX diagnosis criteria included typical chest pain, abnormal exercise ECG, and angiographically normal coronary arteries.
  • Factor XIII gene polymorphism was analyzed using the CVD Strip Assay commercial kit.

Main Results:

  • The FXIII Val/Leu + Leu/Leu mutation occurred significantly more often in CSX patients (43%) compared to controls (19%) (p=0.02).
  • The Leu allele frequency was also higher in the patient group (23.5% vs. 11.1%, p=0.04).
  • Multivariate analysis identified FXIII Val34Leu mutation (OR=3.42) and smoking (OR=3.33) as independent predictors of CSX.

Conclusions:

  • This study provides evidence supporting an association between the factor XIII Val34Leu polymorphism and cardiac syndrome X.
  • The FXIII Val34Leu variant may represent a genetic risk factor for CSX.
  • Further research is warranted to elucidate the precise mechanisms linking FXIII polymorphism to CSX pathogenesis.
Abstract

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