title: AGT*M235T polymorphism in acute ischemic cardiac dysfunction: the gisca project.
abstract: BACKGROUND
  AGT*M235T polymorphism has been associated with high serum angiotensinogen (AGT) levels, systemic hypertension and cardiac dysfunction (CD).
  
  
  OBJECTIVE
  To test the hypothesis of AGT*M235T polymorphism being associated with the risk of developing cardiac dysfunction (heart failure or asymptomatic left ventricular systolic dysfunction) after acute coronary syndrome (ACS) during hospitalization.
  
  
  METHODS
  A total of 363 patients (mean age of 62 ± 12 years), of whom 233 (64%) were men and 130 (36%) were women, all from the same cohort and hospitalized for ACS, were studied. Clinical and genetic data from the 117 (32.2%) patients who developed cardiac dysfunction (case group) were compared to those of the 246 (67.8%) who did not develop this condition (control group). The AGT*M235T polymorphism was determined by sequence analysis and was in Hardy-Weinberg equilibrium.
  
  
  RESULTS
  There was a significant difference in the distribution of genotypes among women, with a predominance of the *235MM genotype in the control group (p = 0.001) and of the *235T allele in the case group. In the logistic regression models, the diagnosis of anterior wall myocardial infarction at admission was related to an increased risk of CD in both genders, whereas unstable angina at admission.; absence of the *235T allele; blood glucose <100 mg/dl; use of betablocker; serum creatinine level < 1.5 mg/dl;heart rate range > 60 and < 90 bpm; and current cigarette smoking were related to a lower risk of CD.
  
  
  CONCLUSIONS
  This study suggests that the absence of the AGT *235T allele contributes to a reduced risk of cardiac dysfunction after acute coronary syndrome.
authors.affiliation: Universidade Federal Fluminense, Rio de Janeiro, RJ, Brasil. cgsaud@cardiol.br
authors.forename: Claudia Guerra Murad
authors.initials: CG
authors.lastname: Saud
authors.forename: Amália Faria Dos
authors.initials: AF
authors.lastname: Reis
authors.forename: Arlisa Monteiro de Castro
authors.initials: AM
authors.lastname: Dias
authors.forename: Rosemery Nunes
authors.initials: RN
authors.lastname: Cardoso
authors.forename: Ana Cristina Klem Vargas
authors.initials: AC
authors.lastname: Carneiro
authors.forename: Leandro Pereira de
authors.initials: LP
authors.lastname: Souza
authors.forename: Ana Beatriz Monteiro
authors.initials: AB
authors.lastname: Fonseca
authors.forename: Georgina Severo
authors.initials: GS
authors.lastname: Ribeiro
authors.forename: Carlos Augusto Cardozo de
authors.initials: CA
authors.lastname: Faria
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis / Q000235:genetics*; D000328:Adult; D000483:Alleles; D000808:Angiotensinogen / Q000097:blood / Q000235:genetics*; D016022:Case-Control Studies; D004452:Echocardiography; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000235:genetics; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics; D011110:Polymorphism, Genetic; D055815:Young Adult
chemical_list: D000808:Angiotensinogen