title: ACE/DD genotype is associated with hemostasis balance disturbances reflecting hypercoagulability and endothelial dysfunction in patients with untreated hypertension.
abstract: BACKGROUND
  Angiotensin-converting enzyme (ACE) gene polymorphism has been associated with an increased incidence of myocardial infarction. Recent studies have investigated a potential influence of ACE gene polymorphism on fibrinolysis or endothelial function. It has been previously established that essential hypertension is accompanied by endothelial dysfunction and fibrinolytic balance disorders. The aim of our study was to study the relation between ACE gene polymorphism and fibrinolytic/hemostatic factors as well as endothelial cell damage markers in patients with hypertension.
  
  
  METHODS
  The following parameters were evaluated in 104 patients with previously untreated hypertension: plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) antigen, fibrinogen, D-dimer, and von Willebrand factor (vWF). The genotype of the ACE gene was also determined (by the polymerase chain reaction method), and patients were characterized according to the observed alleles as deletion/deletion (DD), insertion/insertion (II), or insertion/deletion (ID).
  
  
  RESULTS
  Those with DD genotype (n = 42) had significantly higher plasma levels of PAI-1 antigen (P =. 012), tPA antigen (P =.0001), fibrinogen (P =.0002), D-dimer (P =. 0001) and vWF (P =.0004) compared with ID (n = 30) or II (n = 32) genotypes. The ACE gene genotypes appeared to be significant predictors for plasma PAI-1 antigen, tPA antigen, fibrinogen, D -dimer, and vWF even after adjustment for age, sex, body mass index, triglyceride and cholesterol levels, and blood pressure.
  
  
  CONCLUSIONS
  Our findings suggest that the ACE/DD genotype is associated with hemostasis balance disturbances reflecting hypercoagulability and endothelial damage in patients with untreated hypertension.
authors.affiliation: Laikon General Hospital, National University of Athens, Athens, Greece. gstav@hol.gr
authors.forename: T K
authors.initials: TK
authors.lastname: Makris
authors.forename: G A
authors.initials: GA
authors.lastname: Stavroulakis
authors.forename: U G
authors.initials: UG
authors.lastname: Dafni
authors.forename: A E
authors.initials: AE
authors.lastname: Gialeraki
authors.forename: P G
authors.initials: PG
authors.lastname: Krespi
authors.forename: A N
authors.initials: AN
authors.lastname: Hatzizacharias
authors.forename: C G
authors.initials: CG
authors.lastname: Tsoukala
authors.forename: J S
authors.initials: JS
authors.lastname: Vythoulkas
authors.forename: M K
authors.initials: MK
authors.lastname: Kyriakidis
mesh_terms: D001777:Blood Coagulation / Q000235:genetics; D001778:Blood Coagulation Disorders / Q000235:genetics*; D001779:Blood Coagulation Factors / Q000235:genetics / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012307:Risk Factors
chemical_list: D001779:Blood Coagulation Factors; D007703:Peptidyl-Dipeptidase A