title: Prognostic value of ACE I/D, AT1R A1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms in myocardial infarction.
abstract: BACKGROUND
  Coronary artery disease (CAD) has turned into a prevalent cause of morbi-mortality contributing some polymorphisms in the recurrence of major adverse cardiac events (MACE).
  
  
  METHODS
  Three hundred and fifty six patients with first myocardial infarction (MI) were followed up during a 60-month period to find out if ACE I/D, AT1R A1166C, PAI-I 4G/5G and GPIIIa a1/a2 polymorphisms, in combination with other classical cardiovascular risk factors, can contribute to the relapse of MACE.
  
  
  RESULTS
  Two hundred and eighty five (80.1%) men and 71 (19.9%) women were followed up after first MI. The primary clinical endpoint, a composite of MACE, was reached in 106 (29.8%) patients. In the Cox univariate survival analysis those risk factors influencing a poorer prognosis were age (p = 0.004), a positive family history of CAD (p = 0.007), diabetes (p = 0.004), smoking (p = 0.024), fibrinolytic therapy (p = 0.012) and having 2 or 3 vessels CAD (p = 0.046). Cox proportional hazards regression model showed that patients with the DD genotype had a 1.5 increased risk of having an unfavorable outcome when compared with No-DD genotype patients (RR 1.561, 95% CI 1.048-2.326, p = 0.028) and that patients with the ACE DD genotype plus the AT1R No-AA genotype, the GPIIIa No-a1a1 genotype or a combination of both, had a twice higher risk than any other genotype of MACE in the follow-up (RR 1.978, 95% CI 1.286-3.043, p = 0.002).
  
  
  CONCLUSIONS
  Patients with the ACE DD genotype plus 1 or 2 unfavorable genotypes, the AT1R No-AA, the GPIIIa No-a1a1 or a combination of both, have twice higher the risk of MACE during their clinical follow-up.
authors.affiliation: Cardiology Service, Insular-Materno Infantil University Hospital, Las Palmas de Gran Canaria, Spain. efrencardio@gmail.com.
authors.forename: Efrén
authors.initials: E
authors.lastname: Martínez-Quintana
authors.forename: Ricardo
authors.initials: R
authors.lastname: Chirino
authors.forename: Vicente
authors.initials: V
authors.lastname: Nieto-Lago
authors.forename: Patricia
authors.initials: P
authors.lastname: Pérez-Jiménez
authors.forename: Laura
authors.initials: L
authors.lastname: López-Ríos
authors.forename: Fayna
authors.initials: F
authors.lastname: Rodríguez-González
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004247:DNA / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D039661:Integrin beta3 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics* / Q000378:metabolism / Q000401:mortality; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D011446:Prospective Studies; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics* / Q000378:metabolism; D012307:Risk Factors; D015996:Survival Rate / Q000639:trends; D013997:Time Factors; D055815:Young Adult
chemical_list: D039661:Integrin beta3; D017395:Plasminogen Activator Inhibitor 1; D044140:Receptor, Angiotensin, Type 1; D004247:DNA; D007703:Peptidyl-Dipeptidase A