Dispersion of repolarization following double and triple programmed stimulation: A clinical study using the monophasic action potential recording technique

Abstract

To study the dispersion of ventricular repolarization following double and triple programmed stimulation and its correlation with the inducibility of ventricular arrhythmias, monophasic action potentials were simultaneously recorded from the right ventricular apex and outflow tract during programmed stimulation in 12 patients with ventricular arrhythmias and a normal QT interval. The time difference between the ends of the two monophasic action potentials were used as a measure of the dispersion of ventricular repolarization, which consists of the activation time difference and the monophasic action potential duration difference. During double and triple programmed stimulation, the dispersion of ventricular repolarization increased significantly with the shortening of the coupling interval but decreased slightly with the shortening of the preceding interval. The induction of the ventricular arrhythmias in these patients was invariably associated with a marked increase in the dispersion of ventricular repolarization. The maximal dispersion of ventricular repolarization was significantly larger in the seven patients with polymorphic ventricular tachycardia and/or ventricular flutter/fibrillation induced than in the four patients with monomorphic ventricular tachycardia induced. Analysis of the two components of the dispersion of ventricular repolarization revealed that the increased dispersion of ventricular repolarization was mainly caused by an increase in the activation time difference in the monomorphic ventricular tachycardia subgroup, and by increases in both the activation time difference and monophasic action potential duration difference in the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricular repolarization is one of the underlying mechanisms accounting for the myocardial vulnerability to ventricular arrhythmias and that repolarization disturbance is important for the genesis of polymorphic ventricular tachycardia/fibrillation.

QT Interval Dispersion in Ventricular Beats: A Noninvasive Marker of Susceptibility to Sustained Ventricular Arrhythmias

“…In the present study, not only the QTd-VPB was significantly greater than QTd-SB, but an even more significant difference was present between QTd-SB and QTd-Vpace. These results show that regional variation in ventricular recovery is more increased following ventricular extrasystoles than during sinus beats and confirm the results of other studies 10,12,13 that have shown that one of the triggering mechanisms of VPBs in sustained VT induction may be a further increase in nonuniformity of repolarization. patients) might have also accounted for these differences.…”

“…We have demonstrated that the shorter the coupling interval of a paced ventricular beat, the greater the QTd. These findings are in agreement with the results of Yuan et al 12 who, using monophasic action potential recordings from two ventricular sites, demonstrated the maximal dispersion of ventricular repolarization occurring 10-20 ms before the ventricular effective refractory period in 11 of the 12 patients studied.…”

“…It has been shown that VPB further increases inhomogeneity of ventricular repolarization and may facilitate initiation of reentrant ventricular arrhythmia. [10][11][12] Accordingly, we hypothesised that QTd in spontaneous (QTd-VPB) or paced (QTd-Vpace) ventricular beats may be superior to QTd-SB in identification of patients with sustained VT.…”

Age- and sex-based reference ranges for non-invasive ventricular repolarisation parameters

“…Human ventricular wall comprises three electrophysiologically and functionally distinct cell types: epicardial, mid‐myocardial and endocardial cells, with M cells showing the longest action potential (AP) duration; the intrinsic differences in AP duration lead to a transmural repolarisation heterogeneity among the layers . In pathological conditions, transmural electrical differences in APs are amplified, with the consequent higher dispersion of repolarisation across the ventricular wall and the increased vulnerability to ventricular arrhythmias …”

“…1 In pathological conditions, transmural electrical differences in APs are amplified, with the consequent higher dispersion of repolarisation across the ventricular wall and the increased vulnerability to ventricular arrhythmias. 2 Dispersion of ventricular repolarisation (DVR) can be assessed non-invasively using a 12-lead surface electrocardiogram (ECG). It has, in fact, been demonstrated, by means of monophasic action potentials recordings, that some electrocardiographic variables involving the terminal part of QT, such as the Tpeak-Tend (Tpe) interval, reflect indirectly DVR.…”