Association of polymorphisms in platelet and hemostasis system genes with acute myocardial infarction

Joshua W Knowles1, Huijan Wang, Haruka Itakura

  • 1Stanford University School of Medicine, Stanford, CA 94305-5405, USA.

American Heart Journal
|November 24, 2007
PubMed

Insights

Genetic variations in coagulation genes may influence acute myocardial infarction (MI) risk. Specific single nucleotide polymorphisms (SNPs) in CD36, ITGB3, and THBD showed associations with MI in coronary artery disease patients.

Area of Science:

  • Cardiovascular Genetics
  • Hemostasis and Thrombosis

Background:

  • Genetic polymorphisms can disrupt the coagulation-fibrinolysis balance.
  • This imbalance may increase susceptibility to acute myocardial infarction (MI) in individuals with coronary atherosclerosis.

Purpose of the Study:

  • To investigate the association between genetic polymorphisms in coagulation system genes and the risk of acute myocardial infarction (MI).
  • To compare the frequency of specific single nucleotide polymorphisms (SNPs) between patients presenting with acute MI and those with stable exertional angina.

Main Methods:

  • Genotyped 49 single nucleotide polymorphisms (SNPs) in 9 coagulation system genes.
  • Enrolled 1375 patients with coronary disease, comparing those with acute MI to those with stable exertional angina.

Main Results:

  • An SNP in CD36 (rs3211956) was more common in acute MI patients (10.5%) vs. stable angina (8.0%), P=.04.
  • Associations for SNPs in ITGB3 and THBD were not statistically significant but showed trends.
  • The CD36 association became marginally significant after adjusting for cardiac risk factors (OR 1.34, P=.053).

Conclusions:

  • Nominal associations were found between four SNPs in platelet glycoprotein and hemostatic genes and acute MI presentation.
  • These findings suggest a potential role for these genetic variations but require validation in larger cohorts.
Abstract

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