Endothelial nitric oxide synthase genotypes modulate peripheral vasodilatory properties after myocardial infarction

Gene. 2015 Sep 1;568(2):165-9. doi: 10.1016/j.gene.2015.05.042. Epub 2015 May 20.


Background: Studies in population genetics suggest an important relationship between the eNOS G894T polymorphism and occurrence of acute myocardial infarction (AMI), with little known on its influence on the post-AMI period.

Aim: To investigate the association of allelic variants produced by the G894T transversion in eNOS (rs1799983) with post-AMI variables.

Methods: Cross-sectional analyses of anthropometric, clinical and laboratory assessments obtained within the first 24h and after 5 and 30 days of the AMI event across T carriers and G homozygotes of eNOS in 371 consecutive cases of AMI with ST-segment elevation admitted to a Brazilian emergency service in cardiology. Genotypes were determined by polymerase chain reaction followed by enzymatic restriction.

Results: Despite no difference between genotypic groups on aspects as Killip-Kimbal classification scores, extension of infarcted mass, lipid profile or pattern of medication use, an increase in serum nitric oxide from admission to day 5 was higher for T carriers (p<0.001). Thirty days post-AMI, peripheral blood flow reserve was larger among T carriers either by flow- (p=0.037) and nitrate-mediated (p=0.040) dilation testing.

Conclusion: Our results suggest an association of the eNOS 894T allele with an apparent improvement in late arterial function in post-AMI patients.

Keywords: Myocardial infarction; Nitric oxide; Polymorphism; Vascular endothelium; Vasodilation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cross-Sectional Studies
  • Female
  • Genetic Association Studies
  • Genotype
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / enzymology*
  • Myocardial Infarction / genetics
  • Myocardial Infarction / physiopathology
  • Nitric Oxide Synthase Type III / genetics*
  • Polymorphism, Single Nucleotide
  • Recovery of Function
  • Vasodilation


  • NOS3 protein, human
  • Nitric Oxide Synthase Type III