title: Electrocardiographic intervals associated with incident atrial fibrillation: Dissecting the QT interval.
abstract: Prolongation of the QT interval has been associated with an increased risk of developing atrial fibrillation (AF), but the responsible mechanism remains unknown.
  
  
  
  The aims of this study were to subdivide the QT interval into its components and identify the resultant electrocardiographic interval(s) responsible for the association with AF.
  
  
  
  Predefined QT-interval components were assessed for association with incident AF in the Atherosclerosis Risk in Communities study using Cox proportional hazards models. Hazard ratios (HRs) were calculated per 1-SD increase in each component. Among QT-interval components exhibiting significant associations, additional analyses evaluating long extremes, defined as greater than the 95thpercentile, were performed.
  
  
  
  Of the 14,625 individuals, 1505 (10.3%) were diagnosed with incident AF during a mean follow-up period of 17.6 years. After multivariable adjustment, QT-interval components involved in repolarization, but not depolarization, exhibited significant associations with incident AF, including a longer ST segment (HR 1.27; 95% confidence interval [CI] 1.14-1.41; P < .001) and a prolonged T-wave onset to T-wave peak (T-onset to T-peak) (HR 1.13; 95% CI 1.07-1.20; P < .001). Marked prolongation of the ST segment (HR 1.31; 95% CI 1.04-1.64; P = .022) and T-onset to T-peak (HR 1.36; 95% CI 1.09-1.69; P = .006) was also associated with an increased risk of incident AF.
  
  
  
  The association between a prolonged QT interval and incident AF is primarily explained by components involved in ventricular repolarization: prolongation of the ST segment and T-onset to T-peak. These observations suggest that prolongation of phases 2 and 3 of the cardiac action potential drives the association between the QT interval and AF risk.
authors.affiliation: Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, Western University, London, Ontario, Canada. Electronic address: jason.roberts@lhsc.on.ca.
authors.forename: Jason D
authors.initials: JD
authors.lastname: Roberts
authors.affiliation: Epidemiological Cardiology Research Center, Wake Forest University School of Medicine, Winston Salem, North Carolina.
authors.forename: Elsayed Z
authors.initials: EZ
authors.lastname: Soliman
authors.affiliation: Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia.
authors.forename: Alvaro
authors.initials: A
authors.lastname: Alonso
authors.affiliation: Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California.
authors.forename: Eric
authors.initials: E
authors.lastname: Vittinghoff
authors.affiliation: Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minnesota.
authors.forename: Lin Y
authors.initials: LY
authors.lastname: Chen
authors.affiliation: Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina.
authors.forename: Laura
authors.initials: L
authors.lastname: Loehr
authors.affiliation: Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, San Francisco, San Francisco, California. Electronic address: greg.marcus@ucsf.edu.
authors.forename: Gregory M
authors.initials: GM
authors.lastname: Marcus
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans
keywords: Arrhythmia; Atrial fibrillation; Electrocardiography; Epidemiology; QT interval