Abstract

The purpose of this study was to evaluate the relationship between electrocardiogram (ECG) QRS fragmentation (fQRS) and right ventricular (RV) endocardial (ENDO) and epicardial (EPI) electroanatomic substrate abnormalities in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). fQRS is frequently observed in patients with ARVC and reflects delayed conduction due to RV fibrosis. A total of 30 consecutive patients met the task force criteria for ARVC (19 men, mean age 41.1 ± 14.3 years) presenting for ventricular tachycardia ablation with detailed RV ENDO and EPI electroanatomic maps were included. Of these, 25 patients had depolarization abnormalities (fragmentation during and/or immediately after the QRS complex [fQRS]) in≥2 contiguous ECG leads. Inferior (II, III, aVF) fQRS was identified in 23 patients, anterior (V1 to V3) in 15patients,and basal superior (I/aVR) in 11 patients. The surface area and anatomic distribution of ENDO and EPI bipolar low-voltage regions (ENDO≤1.5 mV,<0.5 mV "dense scar"/EPI≤1.0 mV) and degree of isolated late potential activity consistent with a marked substrate abnormality were compared to the location of region-specific fQRS. In fQRS patients, ENDO very low bipolar voltage area (27.4 ± 24.9 cm2 [median 19 cm2] vs. 5.8 ± 5.4 cm2 [median 5 cm2]; p= 0.02) and EPI late potential percentage (22.6 ± 9.6% [median 24%] vs. 6.8 ± 3.9% [median 8%]; p= 0.002) were significantly larger than in patients without fQRS. Overall, ENDO and EPI bipolar low voltage area andlate potential density increased as the number of fQRS ECG regions (0 to 3) increased. Inferior fQRS most frequently identified EPI inferior substrate (82% sensitivity, 100% specificity), anterior fQRS identified RV EPI mid-free wall substrate (55% sensitivity, 100% specificity), and basal superior fQRS identified ENDO (45.8% sensitivity, 100% specificity) and EPI (52% sensitivity, 100% specificity) RV outflow tract substrate abnormalities. The extent and distribution of RV voltage substrate abnormalities can be predicted by region-specific ECG depolarization changes in patients with ARVC and ventricular tachycardia.

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