ACE Gene in Egyptian Ischemic Stroke Patients

J Stroke Cerebrovasc Dis. 2016 Sep;25(9):2167-71. doi: 10.1016/j.jstrokecerebrovasdis.2015.05.015. Epub 2016 Jul 25.

Abstract

Background: Angiotensin-1-converting enzyme (ACE) is a crucial player in vascular homeostasis and in the pathogenesis of atherosclerosis and hypertension. The present study was conducted to determine whether there is an association between the ACE insertion/deletion (I/D) polymorphism and ischemic stroke in Egyptian population. Also, we analyzed the ACE gene I/D polymorphism as a risk factor for small-vessel (SV) versus large-vessel (LV) disease.

Methods: Sixty patients with ischemic stroke were included: 30 with SV disease and 30 with LV disease. In addition, a control group of 30 apparent healthy subjects were studied. Clinical assessment, computed tomography, magnetic resonance imaging brain, and genetic study using the polymerase chain reaction of ACE gene were done for all subjects.

Results: We found that the distribution of ACE gene polymorphism frequency was significantly different between the 3 groups. The DD genotype was far more common in stroke patients compared to controls. It was also significantly more common in each of the patient groups compared to controls but rather similar in the 2 patient groups with SV and LV diseases.

Conclusion: We found that the ACE gene deletion/deletion genotype is common in Egyptian patients with non-cardioembolic ischemic stroke but does not appear to be specific neither to SV nor to LV disease.

Keywords: ACE gene; large-vessel disease; leucoaraiosis; small-vessel disease.

MeSH terms

  • Aged
  • Brain Ischemia / complications*
  • Brain Ischemia / diagnostic imaging
  • DNA Mutational Analysis
  • Egypt / epidemiology
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease*
  • Genotype
  • Humans
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Single Nucleotide / genetics*
  • Stroke / diagnostic imaging
  • Stroke / etiology*
  • Stroke / genetics*

Substances

  • Peptidyl-Dipeptidase A