title: The D-allele of the ACE polymorphism is related to increased QT dispersion in 609 patients after myocardial infarction.
abstract: OBJECTIVE
  Prolongation of QT dispersion can be observed in some patients with myocardial infarction and serves as a possible independent risk factor for sudden cardiac death. Angiotensin-converting enzyme (ACE) inhibition has been shown to reduce QT dispersion in myocardial infarction patients. We hypothesized that ACE gene I/D polymorphism, which is known to modulate ACE activity, may also affect QT dispersion after myocardial infarction.
  
  
  RESULTS
  We studied 609 myocardial infarction patients (532 men, aged 56.1+/-0.3; mean 5.5 years after myocardial infarction) from a population-based myocardial infarction register by standardized questionnaire, anthropometry, ECG, echocardiography, and genotyping of ACE I/D polymorphism. In addition, 540 unaffected siblings (251 men, age 54.6+/-0.4 years) of these patients were studied by the same protocol. As compared with their healthy siblings, mean QT dispersion was prolonged in myocardial infarction patients (65.9+/-1.4 ms vs 91.2+/-2.3 ms, respectively, P<0.001). QT dispersion was negatively correlated to left ventricular ejection fraction (P<0.005). The ACE DD-genotype was associated with longer QT dispersion in myocardial infarction patients (103.0+/-4.6 ms vs 81.9+/-4.5 ms in the II group, P<0.001). This association was noted to be strong in multivariate analyses that included age, gender, ejection fraction, left ventricular end-diastolic diameter, medication, and heart rate. In contrast, no association between the ACE DD-genotype and QT dispersion was detected in healthy siblings of myocardial infarction patients.
  
  
  CONCLUSIONS
  Thus, the ACE D-allele may be associated with increased QT dispersion in patients after myocardial infarction but not in healthy subjects. An interaction of myocardial damage and genetic predisposition that both enhance the activity of the renin angiotensin system may decrease the repolarization homogeneity of the heart.
authors: Innere Medizin II, Klinikum der Universität Regensburg, Regensburg, Germany.
authors: A
authors: A
authors: Jeron
authors: C
authors: C
authors: Hengstenberg
authors: S
authors: S
authors: Engel
authors: H
authors: H
authors: Löwel
authors: G A
authors: GA
authors: Riegger
authors: H
authors: H
authors: Schunkert
authors: S
authors: S
authors: Holmer
mesh_terms: D000483:Alleles; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D016022:Case-Control Studies; D016757:Death, Sudden, Cardiac / Q000209:etiology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D005858:Germany / Q000453:epidemiology; D006801:Humans; D008133:Long QT Syndrome / Q000453:epidemiology / Q000209:etiology* / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000150:complications* / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D011159:Population Surveillance; D012042:Registries; D012307:Risk Factors; D011795:Surveys and Questionnaires
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D007703:Peptidyl-Dipeptidase A