Morphological algebraic models of the TU-wave patterns/in idiopathic long QT syndrome

A computer-assisted analysis of the TU-complex morphology was employed to characterize repolarization abnormalities in LQTS and to assess arrhythmic risk. Electrocardiograms (ECGs) were collected from 14 idiopathic LQTS patients (seven without symptoms and seven with a history of syncope or cardiac arrest) and from 14 sex- and age-matched normal subjects. Digitized TU-wave patterns from V2–V6 precordial leads were analyzed. The morphologies of the T and U waves were modeled by an algebraic sum of differences between two pairs of action potential-like curves of different shape and duration so that the whole TU complex was approximated by (S1−S2)+(L1−L2). By finding the best fit model of the digitized TU-wave signal, the amplitude and duration of each decomposition curve were determined for each lead. The following ‘secondary’ parameters were then derived: (a) the ratio between the sum of the amplitudes of the two long (L1 and L2) and the two short (S1 and S2) decomposition curves (A-ratio), (b) the highest A-ratio found in V2 to V6 (A-ratio max), and (c) the model-derived durations of the T-wave, U-wave and TU-complex. Conventional measures of RR and QTc intervals and of QT dispersion did not differ between symptomatic and asymptomatic LQTS patients. Modeled QT interval was significantly longer in the symptomatic than in the asymptomatic LQTS patients and in asymptomatic LQTS patients than in the controls. In addition, symptomatic LQTS patients had a longer S2 and T-wave duration in most leads than normal subjects. Conversely, modeled QU interval and U-wave duration did not significantly differ between the three groups. Compared to normal subjects, the amplitudes of S1, S2, L1 and L2 in the LQTS patients were not significantly different in most leads. A-ratio and A-ratio max were greater in symptomatic than asymptomatic LQTS patients and in the latter than in controls. A cut-off value of 0.90 of A-ratio max separated all symptomatic (1.34±0.38) from all asymptomatic patients (0.60±0.21). Although the correlation between model parameters and cellular substrate is at present unclear, it is possible that the morphological alterations described by the model are related to the arrhythmogenic mechanism(s) of the idiopathic LQTS.