Table 1.
Revised task force criteria in different groups of patients.
Fig 1.
QRS loop of (A) ARVC and (B) control case and (C) loop descriptors.
The QRS loop was constructed from the reconstruction vectors obtained after a principal component analysis. (ARVC: arrhythmogenic right ventricular cardiomyopathy; LD: loop dispersion; PL: loop area)
Table 2.
Baseline patients data.
Table 3.
Analysis of QRS parameters in different types of patients.
Fig 2.
(A) Scatter plot and (B) ROC curves of the IQRSD between V4-V5 and between V6-I.
The IQRSD between V4-V5 separated definite ARVC from RVOT VT (borderline cases), while the IQRSD between V6-1 differentiated Group 1 Group 2. Right panel: ROC curves of IQRSD between V4-V5 and between V6-I. The area under the curve further improved after a combination of the IQRSD between V4-V5 and V6-I. (IQRSD: interlead QRS dispersion; ROC: receiver-operator characteristic).
Fig 3.
(A, B) 3D electroanatomic map and (C, D) corresponding reconstruction vectors of precordial ECG (lower panel) in two ARVC patients.
The spatial inhomogeneity between leads V1 and V2 (C) and between leads V6 and I (D) indicate corresponding epicardial unipolar scar (green area, less than 5.5 mV) at the right ventricle site and left lateral left ventricle, respectively.
Fig 4.
Relationship between IQRSD and LVZ in clinical data.
Positive correlation between maximal normalized IQRSD and proportion of the LVZ in the RV. (LVZ: low-voltage zone; RV: right ventricle)
Fig 5.
Illustration of the change in the QRS morphology and associated IQRSD in computer simulation with respect to ischemia under lead V2 (red dot) and under and between V3 and V4 (blue dot).
(A) heart geometry; (B) QRS changes in precordial leads with ischemia under lead V2; and (C) QRS changes in precordial leads with ischemia under and between V3 and V4. The black lines in (B) and (C) indicate the normal precordial ECG. We delayed the depolarization upstroke of the action potential by 60 msec and reduced the amplitude to two-thirds of the original level to simulate ischemic myocardium as the red and blue traces. When the ischemia was under V2, the IQRSD of V1-V2 and V2-V3 dramatically increased from 48.3 to 66.4 degrees and from 45.1 to 87.6 degrees, respectively. When the ischemia was under and between V2 and V3, the IQRSD of V2-V3 and V3-V4 dramatically increased from 45.1 to 68.4 degrees and from 58.7 to 81.8 degrees, respectively.
Fig 6.
Computation simulation for IQRSD with respect to the proportion of abnormal substrate.
Positive correlation between maximal normalized IQRSD and the area of abnormal substrate in the epicardium.