In a canine model, torsades de pointes was associated with competing activation sequences vying for control of epicardial depolarization, with changes in QRS morphology linked to shifting breakthrough sites.
In a canine model, torsades de pointes is characterized by competing activation sequences from different ventricular sites, explaining the undulating QRS morphology.
A dog model of torsades de pointes (TdP) was developed. Twenty 18-30-kg dogs had cardiopulmonary bypass instituted to maintain stable temperature, perfusion pressure and oxygenation. Quinidine, 30 mg/kg, was then administered and burst ventricular pacing was used to induce arrhythmias. The left anterior descending coronary artery was occluded for 15 minutes and repeat pacing studies were performed. Maps of epicardial activation were made from 27 simultaneously recorded electrograms obtained from 1-mm bipolar electrodes secured to the epicardium with a nylon mesh sock. Arrhythmias in five dogs met criteria for the diagnosis of TdP: All had the characteristic undulating QRS morphology typically associated with TdP, all occurred in the setting of QT prolongation and all ended spontaneously. The epicardial maps demonstrated that each change in QRS morphology was associated with a change in the site of epicardial breakthrough. Those QRS complexes during the transition from one morphology to the next were associated with fusion cycles in which both the old and new sites of epicardial breakthrough were present. In essence, two or more competing activation sequences were vying for control of epicardial depolarization. This conclusion was strengthened by our ability to simulate TdP in the surface ECG and in epicardial maps by simultaneously pacing from two widely separated ventricular sites at slightly different, varying rates.
Bardy et al. (Sat,) conducted a other in Torsades de pointes (n=20). Quinidine, burst ventricular pacing, and coronary occlusion was evaluated on Mechanism of TdP (epicardial activation mapping). In a canine model, torsades de pointes was associated with competing activation sequences vying for control of epicardial depolarization, with changes in QRS morphology linked to shifting breakthrough sites.