Fragmented endocardial signals and early afterdepolarizations during torsades de pointes tachycardia

Abstract

Background: Bradycardia-induced torsade de pointes (TdP) tachycardia in patients with

Mechanisms of torsade de pointes tachycardia in patients with spontaneous high-degree atrioventricular block: A modern look at old data

“…They gave further insight into the mechanisms of initiation and perpetuation of TdP in high-degree AV block. We are potentially dealing with a functional arrhythmogenic substrate, reflected by EGM fragmentations [9] which are not due to a fixed anatomic obstacle such as fibrosis resulting from the sequel of myocardial infarction, but likely to anisotropic propagation creating functional blocks. A relation with the familial forms of LQTS has also been proposed, as not all patients with chronic AV block develop long QT and TdP.…”

“…Therefore, to gain further insight, long-term bipolar ECGs were tape recorded in all, between a negative skin electrode placed in position V1 and a positive one Preliminary results of this study have been previously published. [7][8][9] This study is a more detailed and extended analysis of these previous reports.…”

“…Endocardial data were available from 5 patients, all from the RV apex bipolar electrode, and detailed elsewhere. [8,9] All had an escape electrogram (EGM) with a sharp Purkinje-like potential synchronous with the middle of the QRS, superimposed to a low voltage surrounding signal in 4 of them ( Figure 1B). A similar potential could be observed at the onset of the initiating PVC in case 1 from Figure 1B), preceded by a smooth potential before the QRS onset in continuity with the T wave of the escape beat, interpreted as EAD's from the same region.…”