Dispersion of ventricular repolarization

After a century of use, the electrocardiogram (ECG) remains a standard non-invasive technique for the clinical diagnosis of cardiac abnormalities. The ECG provides considerable information about the anatomy and the physiology of the heart. In the field of rhythm and intra-cardiac conduction analysis, it is without equal. Additional information can even be obtained when computer processing is applied to the ECG signal, for instance in the search of arrhythmic markers such as late potentials from high resolution ECG and heart rate variability from 24-hour holter recording or in clinical diagnosis (Robert et al, 1985; Brochet et al, 1979 and 1990). ECG analysis has thus been proposed to evaluate the arrhythogenic risk in various cardiovascular disorders. It is well established that some characteristics of ventricular disorders. It is well established that some characteristics if ventricular repolarization play an important role in arrhythmogenesis (Merx et al, 1977; Schartz et al, 1978; Mirvis et al, 1985). In the assessment of ventricular repolarization, prolongation of the QT interval duration is known to contribute to some arrhythmia triggering (Schwartz et al, 1985; Surawicz et al, 1987). Recently, the variability of repolarization duration has emerged as a new marker of the vulnerability of developing ventricular tachyarrhythmias.
Several experimental studies have demonstrated that non-uniform recovery of excitability was an important factor in the triggering of ventricular arrhythmias (Han et al, 194 and 1966). The asynchrony of recovery of excitability with increased dispersion of refractory periods within the myocardium has been associated with a lowered ventricular fibrillation threshold (Han et al, 1966).
The hypothesis that heterogeneous repolarization process plays an important role in the genesis of ventricular arrhythmias was further confirmed by other experimental investigations and some clinical studies using an invasive assessment of ventricular repolarization such as electrophysiological studies, ventricular tachycardia induction protocols (Kuo et al, 1983; Caugh et al, 1985; Vassalo et al, 1988), endothelial and epicardial mapping (Franz et al, 1987; Cowan et al, 1988). Repolarization dispersion can also be measured non invasively by recording multilead body potential mapping (Sylven et al, 1984; De Ambroggi et al, 1986).
Recently, the inhomogeneity of recovery periods has been evaluated non-invasively by measuring the repolarization duration in several electrocardiographic leads recorded simultaneously. This interlead variability of the repolarization times was first described for the QT interval (Day et al, 1990; Higham et al, 1992). The concept that QT interlead variability reflects the dispersion of ventricular repolarization is supported by a close correlation between changes in the dispersion of repolarization from ventricular monophasic action potential recordings and changes in QT interval variation produced by ventricular pacing (Sylven et al, 1984; De Ambroggi et al, 1986, Higham et al, 1993). Dispersion of ventricular repolarization was defined as the difference between the longest and the shortest QT interval measured on the 12 lead ECG. Later on, other intervals have been porposed in the assessment of repolarization dispersion, each interval addressing a particular part of the whole recovery process (Zareba et al, 1994). Dispersion of ventricular repolarization has thus been proposed as a new non-invasive marker of ventricular arrhythmias and sudden death. This parameter was also found to be useful in the monitoring of antiarrhythmic drug effects. It is well known that class Ia antiarrhythmic drugs prolong global repolarization times (Strasberg et al, 1981; Bauman et al, 1984). However, in patients who do not develop class Ia drug-induced tachyarrhythmias, this effect is regionally homogeneous as reflected in the absence or an increase in QT dispersion, while in those who develop ventricular arrhythmias, QT interval prolongation was accompanied by an increase in QT dispersion. Furthermore, amiodarone and sotalol which prolong ventricular repolarization duration reduce QT dispersion (Day et al, 1991; Hii et al, 1992)