title: QT dispersion does not represent electrocardiographic interlead heterogeneity of ventricular repolarization.
abstract: BACKGROUND
  QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals.
  
  
  RESULTS
  Seventy-eight normal subjects (47+/-16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38+/-15 years, 21 women), 72 dilated cardiomyopathy patients (DCM; 48+/-15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63+/-12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). QTd was 33.6+/-18.3, 47.0+/-19.3, 34.8+/-21.2, and 57.5+/-25.3 msec in normals, HCM, DCM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%+/-0.031%, 0.067%+/-0.067%, 0.112%+/-0.154%, and 0.186%+/-0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS, other P < 0.006). The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively.
  
  
  CONCLUSIONS
  Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it.
authors.affiliation: Department of Cardiological Sciences, St. George's Hospital Medical School, London, United Kingdom. m.malik@sghms.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Malik
authors.forename: B
authors.initials: B
authors.lastname: Acar
authors.forename: Y
authors.initials: Y
authors.lastname: Gang
authors.forename: Y G
authors.initials: YG
authors.lastname: Yap
authors.forename: K
authors.initials: K
authors.lastname: Hnatkova
authors.forename: A J
authors.initials: AJ
authors.lastname: Camm
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology; D012016:Reference Values; D012146:Rest; D016683:Supine Position; D016276:Ventricular Function