title: [Does a genetic predisposition for infarction expansion exist? Evaluation of genetic polymorphisms of the renin-angiotensin system].
abstract: Aim of this study is to carry out a genetic analysis of polymorphisms of the renin-angiotensin system in a genetically homogeneous population, in patients with and without myocardial infarction (AMI) expansion and to evaluate the influence of non genetic, mechanical factors. The study was conducted on 299 patients with first AMI. Ecocardiography studies were performed on all patients on day 1 and 3 from the onset of AMI and before discharge. Eighty-four patients were excluded because of inadequate quality of echocardiograms and 215 (163 males, 52 females) were admitted. Of these, 157 had no evidence of AMI expansion (EXP-) while 58 had expansion (EXP+). DNA was extracted by standard methods from blood samples. Age and gender had no influence on AMI expansion. Anterior infarction (p < 0.000001) and Q-wave infarction (p < 0.00002) were found more frequently in EXP+. Peak of creatine phosphokinase was higher in EXP+ than in EXP- (p < 0.00001). The percent of patients treated with thrombolysis or with hypertension and/or left ventricular hypertrophy was not significantly different in the two groups. AGT MT235 polymorphism of angiotensinogen gene, I/D polymorphism of ACE gene and AT1 A1166C of AT1 receptor of angiotensin II were not significantly different in two groups. Stratified analysis showed that in patients with anterior AMI (n = 87), with a higher risk of AMI expansion, there is a significant difference (p < 0.02) in ACE genotype between EXP- and EXP+. Odds ratio assuming the dominant effect of I allele (II+ ID < DD) was 3.35 (confidence interval 1.41-7.56) with increased risk of expansion. More extension studies are need to verify if these results can contribute to early identification of patients at higher risk and to optimize therapeutic approach.
authors.affiliation: Istituto di Cardiologia, Università degli Studi, Cagliari.
authors.forename: N
authors.initials: N
authors.lastname: Zedda
authors.forename: E
authors.initials: E
authors.lastname: Onnis
authors.forename: A
authors.initials: A
authors.lastname: Angius
authors.forename: F
authors.initials: F
authors.lastname: Balata
authors.forename: P A
authors.initials: PA
authors.lastname: Cherchi
authors.forename: G
authors.initials: G
authors.lastname: Sole
authors.forename: N
authors.initials: N
authors.lastname: Olla
authors.forename: D
authors.initials: D
authors.lastname: Poddie
authors.forename: A
authors.initials: A
authors.lastname: Cao
authors.forename: A
authors.initials: A
authors.lastname: Cherchi
authors.forename: M
authors.initials: M
authors.lastname: Pirastu
mesh_terms: D000368:Aged; D000483:Alleles; D000804:Angiotensin II / Q000235:genetics; D000808:Angiotensinogen / Q000235:genetics; D015984:Causality; D016001:Confidence Intervals; D004452:Echocardiography; D005260:Female; D005796:Genes; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000235:genetics*; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011945:Receptors, Angiotensin / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics*
chemical_list: D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A