title: Role of tissue plasminogen activator and plasminogen activator inhibitor polymorphism in myocardial infarction.
abstract: A case-control association study on 229 Myocardial Infarction (MI) patients and 217 healthy controls was carried out to determine the role of tissue-plasminogen activator (t-PA) (Alu-repeat insertion (I)/deletion (D)) and plasminogen activator inhibitor (PAI-1) (4G/5G insertion/deletion) polymorphisms with MI in the Pakistani population. In MI patients the genotype distribution of the PAI-1 gene was not found to be different when compared with the unaffected controls (P>0.05, χ2=1.03). The risk allele 4G was also not associated with MI (P>0.05, χ2=0.46, odds ratio (OR)=1.1 (95% confidence interval (CI)=0.84-1.43), P>0.05). Similarly, the genotype frequencies of t-PA I/I, I/D and D/D were not different from the unaffected controls (P>0.05, χ2=1.60), and the risk allele "I" was not found to be associated with MI (P>0.05, χ2=1.35, OR=0.86 (95% CI=0.66-1.11), P>0.05). However, when the data were distributed along the lines of gender a significant association of the 4G/4G PAI-1 genotype was observed with only the female MI patients (P<0.05, z-test=2.21). When the combined genotypes of both the polymorphisms were analyzed, a significant association of MI was observed with the homozygous DD/4G4G genotype (P<0.01, z-test=2.61), which was specifically because of the female samples (P=0.01, z-test=2.53). In addition smoking (P<0.001, χ2=13.52, OR=3.45 (95% CI=1.77-6.94)), diabetes (P<0.001, χ2=22.45, OR=8.89 (95% CI=2.96-29.95)), hypertension (OR=7.76 (95% CI=2.88-22.68), P<0.001) family history (P<0.001, χ2=13.72, OR=3.7 (95% CI=1.71-8.18)) and lower HDL levels (P<0.05) were found to be significantly associated with the disease. In conclusion the PAI-1 gene polymorphism was found to have a gender specific role in the female MI patients.
authors.affiliation: Department of Biosciences, COMSATS Institute of Information Technology, Park Road, Islamabad, 45600, Pakistan.
authors.forename: Waqas
authors.initials: W
authors.lastname: Ahmed
authors.forename: Meera
authors.initials: M
authors.lastname: Malik
authors.forename: Imran
authors.initials: I
authors.lastname: Saeed
authors.forename: Amina Ali
authors.initials: AA
authors.lastname: Khan
authors.forename: Ahmed
authors.initials: A
authors.lastname: Sadeque
authors.forename: Umar
authors.initials: U
authors.lastname: Kaleem
authors.forename: Nuzhat
authors.initials: N
authors.lastname: Ahmed
authors.forename: Muhammad
authors.initials: M
authors.lastname: Ajmal
authors.forename: Maleeha
authors.initials: M
authors.lastname: Azam
authors.forename: Raheel
authors.initials: R
authors.lastname: Qamar
mesh_terms: D008076:Cholesterol, HDL / Q000097:blood; D004587:Electrophoresis, Agar Gel; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D054643:INDEL Mutation / Q000235:genetics; D008297:Male; D009203:Myocardial Infarction / Q000235:genetics*; D016017:Odds Ratio; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012307:Risk Factors; D012907:Smoking; D010959:Tissue Plasminogen Activator / Q000037:antagonists & inhibitors / Q000235:genetics*
chemical_list: D008076:Cholesterol, HDL; D017395:Plasminogen Activator Inhibitor 1; D010959:Tissue Plasminogen Activator