Simulated torsade de pointes - The role of conduction defects and mechanism of QRS rotation

Citation
Ja. Abildskov et Rl. Lux, Simulated torsade de pointes - The role of conduction defects and mechanism of QRS rotation, J ELCARDIOL, 33(1), 2000, pp. 55-64
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF ELECTROCARDIOLOGY
ISSN journal
00220736 → ACNP
Volume
33
Issue
1
Year of publication
2000
Pages
55 - 64
Database
ISI
SICI code
0022-0736(200001)33:1<55:STDP-T>2.0.ZU;2-F
Abstract
A possible mechanism of torsade de pointes consisting of moving sites of re entry in the presence of disparate recovery of excitability has been previo usly proposed. This study evaluates the role of conduction defects in that mechanism. A computer model that simulated propagation, cycle length depend ent recovery of excitability, and slow propagation during incomplete recove ry and in conduction defects was used. Localized conduction defects consist ing of slow propagation were shown to allow reentry at changing locations i n the presence of uniform recovery properties. Later activation within defe cts resulted in later recovery, which permitted independent antegrade propa gation adjacent to the defects. Retrograde propagation in the defects then resulted in reentry. The location of serial reentry changed because retrogr ade propagation and antegrade recovery had opposing directions and met dist al to the origin of antegrade excitation. This mechanism was similar to tha t produced by disparate recovery and the combination of conduction defects and disparate recovery permitted the mechanism to occur with less marked di sparity than otherwise required. The study also showed bidirectional serial reentry around a localized conduction defect or region of disparate recove ry which resulted in relation of QRS peaks around the isoelectric line. The study provided evidence that either conduction defects or disparate recove ry of excitability may be a substrate for torsade de pointes. It also indic ated that combination of these factors might permit torsade de pointes when neither alone does so. This provides a possible explanation for the specia l propensity of quinidine and other drugs that slow conduction as well as p rolong recovery to result in torsade de pointes. Findings also suggested a more explicit mechanism for rotation of QRS peaks about the electrocardiogr am baseline than was previously available.