title: [Study of the intronic polymorphism of the angiotensin 1 converting enzyme among coronary Tunisians].
abstract: BACKGROUND
  The acute coronary syndromes (ACS) are classified among the major causes of mortality in the industrialized countries. The increased angiotensin I converting enzyme (ACEI) activity related to a genetic polymorphism constitutes a hereditary predisposition to these syndromes.
  
  
  OBJECTIVE
  Evaluate the ACEI activity in Tunisian patients with coronary heart disease, and investigate the association between this activity and an intronic deletion of 287 pb on the intron 16 of the ACEI gene.
  
  
  METHODS
  Seventy-two coronary patients and 34 control subjects are recruited for our study. ACEI activity was measured by kinetic method. The intronic deletion was identified by PCR technique.
  
  
  RESULTS
  An increased activity of ACEI was observed in patients compared with control subjects (84.38 ± 33.83 UI/L vs 59.06 ± 18.2 UI/L, P=10(-5)). The molecular study showed a raised relative frequency of D/D genotype (51.4%) among patients, whereas among the witnesses, I/I genotype prevailed (62%). D/D genotype is always associated with highest ACEI activity for the patients and the control subjects.
  
  
  CONCLUSIONS
  The molecular studies and the biochemical investigations of the various parameters of cardiovascular risk (including the ACEI) direct towards a better treatment.
authors.affiliation: Laboratoire de biochimie, service de biochimie, CHU Farhat Hached, Sousse, Tunisie. gaddour83@yahoo.fr
authors.forename: A
authors.initials: A
authors.lastname: Chalghoum
authors.forename: Y
authors.initials: Y
authors.lastname: Noichri
authors.forename: L
authors.initials: L
authors.lastname: Chkioua
authors.forename: I
authors.initials: I
authors.lastname: Gammoudi
authors.forename: A
authors.initials: A
authors.lastname: Dandana
authors.forename: H
authors.initials: H
authors.lastname: Chahed
authors.forename: S
authors.initials: S
authors.lastname: Khelil
authors.forename: G
authors.initials: G
authors.lastname: Jeridi
authors.forename: B
authors.initials: B
authors.lastname: Baudin
authors.forename: S
authors.initials: S
authors.lastname: Ferchichi
authors.forename: A
authors.initials: A
authors.lastname: Miled
mesh_terms: D054058:Acute Coronary Syndrome / Q000175:diagnosis / Q000235:genetics*; D000328:Adult; D000368:Aged; D000809:Angiotensins / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007438:Introns / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D012016:Reference Values; D012307:Risk Factors; D014416:Tunisia
chemical_list: D000809:Angiotensins