title: Genetic ACE I/D polymorphism and recurrence of atrial fibrillation after catheter ablation.
abstract: BACKGROUND
  The angiotensin-converting enzyme (ACE) deletion allele, ACE D, is associated with increased cardiac ACE activity, cardiac fibrosis, and adverse outcomes in cardiovascular disease and has been linked with failure of antiatrial fibrillation (anti-AF) drug treatment. This study tested the hypothesis that the ACE gene insertion/deletion polymorphism associates with AF recurrence after catheter ablation.
  
  
  RESULTS
  In 238 consecutive patients (69% male; mean age, 58±11 years) undergoing catheter ablation of paroxysmal (59%) or persistent (41%) AF, the ACE insertion/deletion polymorphism was genotyped using polymerase chain reaction. After a blanking period of 3 months, AF recurrence (defined as any atrial arrhythmia lasting ≥30 s) was detected using serial 7-day Holter ECG recordings after 3, 6, and 12 months. AF recurrence was observed in 39% and was associated with persistent AF, longer history of AF, previous antiarrhythmic drug use, previous use of diuretics, increased left atrial diameter, increased left ventricular end-diastolic diameter, additional linear ablation lesions, and ACE DD polymorphism. In multivariable analysis, left atrial diameter (odds ratio, 1.111; 95% confidence interval, 1.040-1.187; P=0.002) and ACE DD genotype (odds ratio, 2.251; 95% confidence interval, 1.056-4.798; P=0.036) remained predictors for AF recurrence.
  
  
  CONCLUSIONS
  Left atrial enlargement and the ACE DD polymorphism are predictors for AF recurrence after catheter ablation. The association between the ACE DD polymorphism and AF recidivism supports the use of genetic data for predicting response to AF therapies and highlights the role of fibrosis in AF development.
authors.affiliation: Department of Electrophysiology, and Department of Cardiology, Heart Center, Leipzig, Germany; and Department of Medicine, Vanderbilt University Medical Center, Nashville, TN.
authors.forename: Laura
authors.initials: L
authors.lastname: Ueberham
authors.forename: Andreas
authors.initials: A
authors.lastname: Bollmann
authors.forename: Moore Benjamin
authors.initials: MB
authors.lastname: Shoemaker
authors.forename: Arash
authors.initials: A
authors.lastname: Arya
authors.forename: Volker
authors.initials: V
authors.lastname: Adams
authors.forename: Gerhard
authors.initials: G
authors.lastname: Hindricks
authors.forename: Daniela
authors.initials: D
authors.lastname: Husser
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000201:enzymology / Q000235:genetics / Q000601:surgery*; D017115:Catheter Ablation / Q000009:adverse effects*; D016009:Chi-Square Distribution; D015716:Electrocardiography, Ambulatory; D005260:Female; D017353:Gene Deletion; D020022:Genetic Predisposition to Disease; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016254:Mutagenesis, Insertional; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D010641:Phenotype; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D012008:Recurrence; D012042:Registries; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A
keywords: ACE I/D genotype; ACE polymorphism; atrial fibrillation; catheter ablation; genetics; polymorphism, genetic