The presence of late potentials and delayed activation of ventricular myocardium detected in the SAECG is considered to represent slowed ventricular conduction, which is a substrate for reentrant tachyarrhyth mias (Fig. 13.4). In the first reported series of patients with this disease, late potentials were recorded in 81% of patients by Marcus, Fontaine et al. . In the 151 patients described by Wichter et al. ,late potentials were found in 41%. Kinoshita et al.  analyzed the SAECG in 28 patients with ARVC/D and 35 age-matched normal subjects at two different high-pass filter settings, 25 Hz and 40 Hz. Positive SAECG criteria were found in 20 (71%) and 18 (64%) patients at filter settings of 25 Hz and 40 Hz, respectively. Nazir et al.  also indicated that detection of late potentials in ARVC/D can be improved by employing a high-pass filter of 25 Hz and specifically looking for changes in the Z leads.
As with other ECG markers, there is a correlation between abnormal SAECG values and the extent of right ventricular disease. Nasir et al.  reported that a positive SAECG predicted inducibility of sustained VT during programmed electrical stimulation testing. They performed electrophysiological studies in 40 pa
tients (37±12 years) with ARVC/D. Of the 31 without bundle branch blocks, 21 (76%) had inducible mono-morphic VT. At an fQRS >110 msec the sensitivity of an fQRS >110 msec was 91% to predict inducibility of VT; the specificity was 90%, and the predictive value was 90%. In general, the larger the right ventricular size, the greater the possibility of inducing VT/VF at electrophysiological study and of having sustained ventricular arrhythmias. However, data on arrhythmic risk stratification using signal averaged ECG in ARVC/D are limited . Recently, Pezawas et al.  reported that an abnormal SAECG and decreased left ventricular ejection fraction were statistically significant predictors for VT recurrence by multivariate analysis. Folino et al.  found that patients with ARVC/D who have sustained VT tend to have longer fQRS. Therefore, the presence of an abnormal SAECG might be considered as risk factor, although larger studies with long-term follow-up are needed to determine the predictive value of SAECG in ARVC/D.
It is important to realize that the definitions of abnormal values of SAECG parameters were derived for the purpose of risk stratification of sudden death and ventricular arrhythmias in postinfarction patients. These values may not apply to identification of abnormal SAECG when evaluating young subjects suspected of ARVC/D. Recently, Marcus et al.  investigated this topic and based on published literature of the SAECG of normal subjects, gender- and recording device-specific criteria for SAECG parameters were proposed. These proposed SAECG criteria require evaluation and validation in future studies.
dispersion for risk stratification. The value of QT dispersion as an arrhythmic marker in ARVC/D is controversial. Benn et al.  found increased QT dispersion in ARVC/D patients, without significant differences between patients considered at low and high risk for life-threatening arrhythmias. Peters et al. , analyzing ARVC/D patients with sustained VT who had the overt form of disease, did not find an increased QT dispersion. However, they demonstrated that repolarization abnormalities were present at body surface mapping and might be related to the occurrence of ventricular arrhythmias. In the series of Turrini et al. , QT dispersion was significantly greater in the patients who died suddenly as compared to those presenting different arrhythmic profiles. A cut-off value for QT dispersion >65 ms was associated with a high risk of sudden death with a sensitivity of 85% and a specificity of 75%. However, in this report, QT dispersion was not an independent predictor of high arrhythmic risk at multivari-ate analysis. In the series of Nasir et al. , QT dispersion >65 ms did not discriminate patients with spontaneous and/or induced sustained ventricular arrhythmias from those without. Notably, the localized form of ARVC/D showed a similar frequency of QT dispersion as compared with the diffuse form of the disease. Interestingly, in ARVC/D, an increased QT dispersion showed a similar frequency of negative T waves in V1-V3, which is a marker of repolarization abnormalities [15, 18]. It is important to stress that QRS dispersion is considered as the major determinate of QT dispersion.
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