E-selectin is associated with stable angina and myocardial infarction in a sample of Kurdish population

Lajan Qasim Rahman1, Ruqaya Muhammad Ghareeb2

  • 1College of Medicine, Hawler Medical University, Erbil, Kurdistan Region- Iraq. lajan.qasim@hmu.edu.krd.

Insights

The E-selectin gene polymorphism 7170G>C is linked to ischemic heart disease. Genotype CC was more prevalent in stable angina patients, suggesting a role in cardiovascular disease outcomes.

Area of Science:

  • Cardiovascular Genetics
  • Molecular Biology
  • Immunology

Background:

  • Endothelial dysfunction is a primary driver of Coronary Artery Disease (CAD).
  • Leukocyte adhesion to the endothelium is an early marker of arteriosclerosis, regulated by selectins.
  • E-selectin gene polymorphisms have been associated with ischemic heart disease (IHD).

Purpose of the Study:

  • To investigate the association between E-selectin gene polymorphisms and ischemic heart disease (IHD).
  • To determine the functional impact of the E-selectin gene polymorphism 7170G>C in Iraqi patients with IHD.
  • To analyze the relationship between this polymorphism and different clinical outcomes of cardiovascular disease.

Main Methods:

  • Study involved 200 Iraqi patients and controls from Erbil City.
  • Participants were categorized into stable angina pectoris (SAP), myocardial infarction (MI), and healthy control groups.
  • Sanger sequencing was used to analyze the E-selectin gene polymorphism 7170G>C.

Main Results:

  • The E-selectin 7170G>C polymorphism was significantly associated with stable angina (SAP) and myocardial infarction (MI).
  • Genotype CC was found more frequently in SAP patients compared to MI and control groups (p<0.05).
  • The C allele was more prevalent in SAP patients (15.7%) than in MI (14.58%) and control (10.8%) groups.

Conclusions:

  • Genetic variations in the E-selectin gene, specifically the 7170G>C polymorphism, significantly influence cardiovascular disease outcomes.
  • The 7170G>C polymorphism may serve as a potential genetic marker for stable angina.
  • Further research is warranted to elucidate the precise mechanisms linking E-selectin gene variations to cardiovascular disease pathogenesis.

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